HAMPTON, N.J., June 14, 2025 (GLOBE NEWSWIRE) -- Celldex Therapeutics, Inc. (NASDAQ:CLDX) today announced data demonstrating that barzolvolimab profoundly improves angioedema at 52 weeks in the Company’s Phase 2 clinical trial in chronic spontaneous urticaria (CSU). Angioedema, characterized by swelling of the deeper dermal layers of the skin and mucous membranes, is a painful, debilitating symptom of CSU that has significant impact on quality of life. It commonly affects the face (lips and eyelids), hands, feet, and genitalia but can also involve the tongue, uvula, soft palate, and pharynx1.

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Basel, 15 June 2025 - Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today new dosing restrictions, effective immediately, for ELEVIDYS™ (delandistrogene moxeparvovec), for non-ambulatory Duchenne muscular dystrophy (DMD) patients, irrespective of age, in both clinical and commercial settings. In the commercial setting, non-ambulatory patients should no longer receive Elevidys. In the clinical trial setting, enrolment and dosing of non-ambulatory patients will be immediately paused until additional risk mitigation measures (e.g. immune modulatory treatment) are implemented in the study protocol. Health authorities, investigators and physicians are being informed so that patient care can be quickly adjusted.

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[Ad hoc announcement pursuant to Art. 53 LR] Roche provides safety update on Elevidys™ gene therapy for Duchenne muscular dystrophy in...

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Media ReleaseCOPENHAGEN, Denmark; June 15, 2025

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Genmab Announces Epcoritamab Investigational Combination Therapy Demonstrates High Response Rates in Patients with Relapsed or Refractory (R/R)...

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– Pharmacology modeling data presented at the European Academy of Allergy & Clinical Immunology (EAACI) Congress describe mechanistic insights for greater potency with verekitug compared to tezepelumab –

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Translational Data Illustrate a Mechanism of Greater Potency with Verekitug, a Novel Antibody Antagonist of the TSLP Receptor

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CAMBRIDGE, Mass., June 15, 2025 (GLOBE NEWSWIRE) -- Intellia Therapeutics, Inc. (NASDAQ:NTLA), a leading clinical-stage gene editing company focused on revolutionizing medicine with CRISPR-based therapies, today announced three-year follow-up data from the Phase 1 portion of the ongoing Phase 1/2 study in patients with HAE after receiving a single dose of lonvoguran ziclumeran (lonvo-z, also known as NTLA-2002). Results were shared in an oral presentation at the European Academy of Allergy and Clinical Immunology (EAACI) Congress 2025, held June 13-16 in Glasgow, United Kingdom.

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New late-breaking data at EAACI showed Dupixent outperformed Xolair across all primary and secondary efficacy endpoints of CRSwNP and in all asthma-related endpoints

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Dupixent® (dupilumab) Demonstrated Superiority Over Xolair® (Omalizumab) in Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) in Patients with...

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EAACI: Dupixent demonstrated superiority over Xolair (omalizumab) in chronic rhinosinusitis with nasal polyps in patients with coexisting asthma in first-ever presented phase 4 head-to-head respiratory study

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ROCKVILLE, Md. and SUZHOU, China, June 15, 2025 (GLOBE NEWSWIRE) -- Ascentage Pharma (NASDAQ: AAPG; HKEX: 6855), a global biopharmaceutical company dedicated to addressing unmet medical needs in cancers, announced that results from 13 studies of its core assets, including the novel drug olverembatinib (HQP1351) and the investigational EED inhibitor APG-5918, have been reported at the 2025 European Hematology Association (EHA) Annual Congress.

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EHA 2025 | Multiple Studies Report Encouraging Data of Olverembatinib in Ph+ ALL

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Basel, 16 June 2025 - Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today its decision to proceed with Phase III development of prasinezumab, an investigational anti-alpha-synuclein antibody, in early-stage Parkinson’s disease. This decision is informed by data from the Phase IIb PADOVA study and ongoing open-label extensions (OLEs) of PADOVA and Phase II PASADENA studies.

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Overview

Spinal stenosis happens when the space inside the backbone is too small. This can put pressure on the spinal cord and nerves that travel through the spine. Spinal stenosis happens most often in the lower back and the neck.

Some people with spinal stenosis have no symptoms. Others may experience pain, tingling, numbness and muscle weakness. Symptoms can get worse over time.

The most common cause of spinal stenosis is wear-and-tear damage in the spine related to arthritis. People who have serious spinal stenosis may need surgery.

Surgery can create more space inside the spine. This can ease the symptoms caused by pressure on the spinal cord or nerves. But surgery can't cure arthritis, so arthritis pain in the spine may continue.

Spinal stenosis often causes no symptoms. When symptoms do happen, they start slowly and get worse over time. Symptoms depend on which part of the spine is affected.

Spinal stenosis in the lower back can cause pain or cramping in one or both legs. This happens when you stand for a long time or when you walk. Symptoms get better when you bend forward or sit. Some people also have back pain.

Spinal stenosis in the neck can cause:

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As the spine ages, bone spurs or herniated disks are more likely to happen. These problems can shrink the amount of space available for the spinal cord and the nerves that branch off of it.

Spinal bones are stacked in a column from the skull to the tailbone. They protect the spinal cord, which runs through an opening called the spinal canal.

Some people are born with a small spinal canal. But most spinal stenosis occurs when something happens to reduce the amount of open space within the spine. Causes of spinal stenosis include:

Most people with spinal stenosis are over age 50. Younger people may be at higher risk of spinal stenosis if they have scoliosis or other spinal problems.

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Spinal stenosis - Symptoms and causes - Mayo Clinic

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In human anatomy, the spinal canal, vertebral canal or spinal cavity is an elongated body cavity enclosed within the dorsal bony arches of the vertebral column, which contains the spinal cord, spinal roots and dorsal root ganglia. It is a process of the dorsal body cavity formed by alignment of the vertebral foramina. Under the vertebral arches, the spinal canal is also covered anteriorly by the posterior longitudinal ligament and posteriorly by the ligamentum flavum. The potential space between these ligaments and the dura mater covering the spinal cord is known as the epidural space. Spinal nerves exit the spinal canal via the intervertebral foramina under the corresponding vertebral pedicles.

In humans, the spinal cord gets outgrown by the vertebral column during development into adulthood, and the lower section of the spinal canal is occupied by the filum terminale and a bundle of spinal nerves known as the cauda equina instead of the actual spinal cord, which finishes at the L1/L2 level.

The vertebral canal is enclosed anteriorly by the vertebral bodies, intervertebral discs, and the posterior longitudinal ligament; it is enclosed posteriorly by the vertebral laminae and the ligamenta flava; laterally, it is incompletely enclosed by the pedicles with the interval between two adjacent pedicles on either side creating an intervertebral foramen (allowing the passage of the spinal nerves and radicular blood vessels).[1]

The vertebral canal progressively narrows inferiorly.[1] It is wider in the cervical region to accommodate the cervical enlargement of the spinal cord.[2][3]

The outermost layer of the meninges, the dura mater, is closely associated with the arachnoid mater which in turn is loosely connected to the innermost layer, the pia mater. The meninges divide the spinal canal into the epidural space and the subarachnoid space. The pia mater is closely attached to the spinal cord. A subdural space is generally only present due to trauma and/or pathological situations. The subarachnoid space is filled with cerebrospinal fluid and contains the vessels that supply the spinal cord, namely the anterior spinal artery and the paired posterior spinal arteries, accompanied by corresponding spinal veins. The anterior and posterior spinal arteries form anastomoses known as the vasocorona of the spinal cord and these supply nutrients to the canal. The epidural space contains loose fatty tissue, and a network of large, thin-walled blood vessels called the internal vertebral venous plexuses.[citation needed]

Spinal stenosis is a narrowing of the canal which can occur in any region of the spine and can be caused by a number of factors. It may result in cervical myelopathy[4] if the narrowed canal impinges on the spinal cord itself.

Spinal canal endoscopy can be used to investigate the epidural space, and is an important spinal diagnostic technique.[5][6]

The spinal canal was first described by Jean Fernel.[citation needed]

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Spinal canal - Wikipedia

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The spinal cord is a long, fragile tubelike structure that begins at the end of the brain stem and continues down almost to the bottom of the spine. The spinal cord consists of bundles of nerve axons forming pathways that carry incoming and outgoing messages between the brain and the rest of the body. The spinal cord contains nerve cell circuits that control coordinated movements such as walking and swimming, as well as urinating. It is also the center for reflexes, such as the knee jerk reflex (see figure Reflex Arc: A No-Brainer).

Like the brain, the spinal cord is covered by 3 layers of tissue (meninges). The spinal cord and meninges are contained in the spinal canal, which runs through the center of the spine. In most adults, the spine is composed of 33 individual back bones (vertebrae). Just as the skull protects the brain, vertebrae protect the spinal cord. The vertebrae are separated by disks made of cartilage, which act as cushions, reducing the forces on the spine generated by movements such as walking and jumping. The vertebrae and disks of cartilage extend the length of the spine and together form the vertebral (spinal) column.

How the Spine Is Organized

Like the brain, the spinal cord consists of gray and white matter.

The gray matter forms a butterfly-shaped center in the cord. The front wings (called anterior or ventral horns) contain motor nerve cells (neurons) which transmit information from the brain or spinal cord to muscles, stimulating movement. The back part of the butterfly wing (called posterior or dorsal horns) contains sensory nerve cells, which transmit sensory information from other parts of the body through the spinal cord to the brain.

The surrounding white matter contains columns of nerve fibers (axon bundles) that carry sensory information to the brain from the rest of the body (ascending tracts) and columns that carry motor impulses from the brain to the muscles (descending tracts).

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Spinal Cord - Brain, Spinal Cord, and Nerve Disorders - MSD ...

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Several factors can contribute to the narrowing of the spinal canal, leading to spinal stenosis. Normally, the vertebral canal provides enough room for the spinal cord, cauda equina, and the exiting nerves. However, aging and age-related changes in the spine, injury, other diseases, or inherited conditions can cause narrowing of the spaces.

Aging and age-related changes in the spine happen over a period of time and slowly cause loss of the normal structure of the spine. They are the most common causes of spinal stenosis. As people age, the ligaments that keep the vertebrae of the spine in place may thicken and calcify (harden from deposits of calcium salts). Bones and joints may also enlarge. When surfaces of the bone begin to project out from the body, these projections are called osteophytes (bone spurs). For example:

Arthritis is also a common cause of spinal stenosis. Two forms of arthritis that may affect the spine are osteoarthritis and rheumatoid arthritis.

The following conditions also may cause spinal stenosis:

Some people are born with a condition that can cause spinal stenosis. These conditions cause the spinal canal to narrow, leading to spinal stenosis. For example:

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Spinal Stenosis Symptoms, Causes, & Risk Factors | NIAMS

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In this section, we will cover the anatomical structure of the spinal cord and vertebral column, spinal nerve organisation, blood supply, motor and sensory pathways, clinical examination principles, myotomes and dermatomes, localisation of spinal cord lesions, and common spinal cord syndromes.

The spinal column encases and protects the spinal cord, which serves as a conduit for motor, sensory, and autonomic signals between the brain and the body.

Clinical examination of spinal cord function involves assessing motor, sensory, and autonomic pathways.

Discrepancy exists between spinal segments and vertebral levels:

Afferent (or sensory) input to the nervous system arrives in the spinal cord via the dorsal root.

Efferents (or motor output) exit via the ventral root.

Descending tracts:

Ascending tracts:

Blood supply

A myotome refers to all the muscles or groups of muscles innervated by the motor horn cells within a segment of the cord.

Localising spinal cord lesions

During and after your examination you should seek answers to the following questions.

Small central lesion:

Large central cord lesion:

Brown-Squard syndrome (hemisection):

Complete transection:

Combined degeneration of the cord:

Tabes dorsalis:

Anterior spinal artery syndrome:

Posterior spinal artery syndrome:

Further reading

Publications

Robert Coni, DO, EdS, FAAN.Vascular neurologist and neurohospitalist and Neurology Subspecialty Coordinator at the Grand Strand Medical Center in South Carolina. Former neuroscience curriculum coordinator at St. Lukes / Temple Medical School and fellow of the American Academy of Neurology. Inmy spare time, I like to play guitar and go fly fishing. | Medmastery | Linkedin |

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Neuro 101: Spinal Cord LITFL Neurology library

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Paralysis Ends Now: Revolutionary Cell Therapy That Repairs Severed Spinal Cords Enters Trials and Begins Restoring Human Mobility  Rude Baguette

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IPS acquired Precision Electric Motor Works in February 2020. Precision, the only EASA-certified full-service repair facility in the tri-state area of New Jersey, New York, and Connecticut, now offers all IPS services and resources.

IPS expands Precisions capabilities in on-site and in-shop services for motors and rotating equipment. With the addition of IPS power management services and distribution resources, Precisions customers can also streamline their vendor management.

Single-source capabilities to respond, rethink, and resolveAs part of IPS, Precision is now aligned with the industrys leading provider of critical infrastructure services. The IPS network covers North America, the Caribbean, the United Kingdom, and Western Europe.

We serve over 30,000 customers competing in multiple markets. These include power generation, utilities, water and wastewater, petrochemicals, air separation, oil and gas, metals, mining, paper, aggregates, cement, hospitals, universities, commercial buildings, and data centers.

Read more about IPS single-source capabilities below.

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Precision Electric Motorworks - Integrated Power Services

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The heart is a muscular organ found in humans and other animals. This organ pumps blood through the blood vessels.[1] The heart and blood vessels together make the circulatory system.[2] The pumped blood carries oxygen and nutrients to the tissue, while carrying metabolic waste such as carbon dioxide to the lungs. In humans, the heart is approximately the size of a closed fist and is located between the lungs, in the middle compartment of the chest, called the mediastinum.[4]

An illustration of the anterior view of the human heart

In humans, the heart is divided into four chambers: upper left and right atria and lower left and right ventricles.[5][6] Commonly, the right atrium and ventricle are referred together as the right heart and their left counterparts as the left heart. In a healthy heart, blood flows one way through the heart due to heart valves, which prevent backflow.[4] The heart is enclosed in a protective sac, the pericardium, which also contains a small amount of fluid. The wall of the heart is made up of three layers: epicardium, myocardium, and endocardium.[8]

The heart pumps blood with a rhythm determined by a group of pacemaker cells in the sinoatrial node. These generate an electric current that causes the heart to contract, traveling through the atrioventricular node and along the conduction system of the heart. In humans, deoxygenated blood enters the heart through the right atrium from the superior and inferior venae cavae and passes to the right ventricle. From here, it is pumped into pulmonary circulation to the lungs, where it receives oxygen and gives off carbon dioxide. Oxygenated blood then returns to the left atrium, passes through the left ventricle and is pumped out through the aorta into systemic circulation, traveling through arteries, arterioles, and capillarieswhere nutrients and other substances are exchanged between blood vessels and cells, losing oxygen and gaining carbon dioxidebefore being returned to the heart through venules and veins. The adult heart beats at a resting rate close to 72 beats per minute. Exercise temporarily increases the rate, but lowers it in the long term, and is good for heart health.

Cardiovascular diseases were the most common cause of death globally as of 2008, accounting for 30% of all human deaths.[12][13] Of these more than three-quarters are a result of coronary artery disease and stroke.[12] Risk factors include: smoking, being overweight, little exercise, high cholesterol, high blood pressure, and poorly controlled diabetes, among others.[14] Cardiovascular diseases do not frequently have symptoms but may cause chest pain or shortness of breath. Diagnosis of heart disease is often done by the taking of a medical history, listening to the heart-sounds with a stethoscope, as well as with ECG, and echocardiogram which uses ultrasound.[4] Specialists who focus on diseases of the heart are called cardiologists, although many specialties of medicine may be involved in treatment.[13]

Structure

Location and shape

The human heart is situated in the mediastinum, at the level of thoracic vertebrae T5T8. A double-membraned sac called the pericardium surrounds the heart and attaches to the mediastinum.[16] The back surface of the heart lies near the vertebral column, and the front surface, known as the sternocostal surface, sits behind the sternum and rib cartilages.[8] The upper part of the heart is the attachment point for several large blood vesselsthe venae cavae, aorta and pulmonary trunk. The upper part of the heart is located at the level of the third costal cartilage.[8] The lower tip of the heart, the apex, lies to the left of the sternum (8 to 9cm from the midsternal line) between the junction of the fourth and fifth ribs near their articulation with the costal cartilages.[8]

The largest part of the heart is usually slightly offset to the left side of the chest (levocardia). In a rare congenital disorder (dextrocardia) the heart is offset to the right side and is felt to be on the left because the left heart is stronger and larger, since it pumps to all body parts. Because the heart is between the lungs, the left lung is smaller than the right lung and has a cardiac notch in its border to accommodate the heart.[8]The heart is cone-shaped, with its base positioned upwards and tapering down to the apex.[8] An adult heart has a mass of 250350 grams (912oz).[17] The heart is often described as the size of a fist: 12cm (5in) in length, 8cm (3.5in) wide, and 6cm (2.5in) in thickness,[8] although this description is disputed, as the heart is likely to be slightly larger.[18] Well-trained athletes can have much larger hearts due to the effects of exercise on the heart muscle, similar to the response of skeletal muscle.[8]

Chambers

The heart has four chambers, two upper atria, the receiving chambers, and two lower ventricles, the discharging chambers. The atria open into the ventricles via the atrioventricular valves, present in the atrioventricular septum. This distinction is visible also on the surface of the heart as the coronary sulcus. There is an ear-shaped structure in the upper right atrium called the right atrial appendage, or auricle, and another in the upper left atrium, the left atrial appendage. The right atrium and the right ventricle together are sometimes referred to as the right heart. Similarly, the left atrium and the left ventricle together are sometimes referred to as the left heart. The ventricles are separated from each other by the interventricular septum, visible on the surface of the heart as the anterior longitudinal sulcus and the posterior interventricular sulcus.

The fibrous cardiac skeleton gives structure to the heart. It forms the atrioventricular septum, which separates the atria from the ventricles, and the fibrous rings, which serve as bases for the four heart valves.[21] The cardiac skeleton also provides an important boundary in the heart's electrical conduction system since collagen cannot conduct electricity. The interatrial septum separates the atria, and the interventricular septum separates the ventricles.[8] The interventricular septum is much thicker than the interatrial septum since the ventricles need to generate greater pressure when they contract.[8]

Valves

The heart, showing valves, arteries and veins. The white arrows show the normal direction of blood flow.

The heart has four valves, which separate its chambers. One valve lies between each atrium and ventricle, and one valve rests at the exit of each ventricle.[8]

The valves between the atria and ventricles are called the atrioventricular valves. Between the right atrium and the right ventricle is the tricuspid valve. The tricuspid valve has three cusps, which connect to chordae tendinae and three papillary muscles named the anterior, posterior, and septal muscles, after their relative positions. The mitral valve lies between the left atrium and left ventricle. It is also known as the bicuspid valve due to its having two cusps, an anterior and a posterior cusp. These cusps are also attached via chordae tendinae to two papillary muscles projecting from the ventricular wall.

The papillary muscles extend from the walls of the heart to valves by cartilaginous connections called chordae tendinae. These muscles prevent the valves from falling too far back when they close.[24] During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight. As the heart chambers contract, so do the papillary muscles. This creates tension on the chordae tendineae, helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria.[8][g]

Two additional semilunar valves sit at the exit of each of the ventricles. The pulmonary valve is located at the base of the pulmonary artery. This has three cusps which are not attached to any papillary muscles. When the ventricle relaxes blood flows back into the ventricle from the artery and this flow of blood fills the pocket-like valve, pressing against the cusps which close to seal the valve. The semilunar aortic valve is at the base of the aorta and also is not attached to papillary muscles. This too has three cusps which close with the pressure of the blood flowing back from the aorta.[8]

Right heart

The right heart consists of two chambers, the right atrium and the right ventricle, separated by a valve, the tricuspid valve.[8]

The right atrium receives blood almost continuously from the body's two major veins, the superior and inferior venae cavae. A small amount of blood from the coronary circulation also drains into the right atrium via the coronary sinus, which is immediately above and to the middle of the opening of the inferior vena cava.[8] In the wall of the right atrium is an oval-shaped depression known as the fossa ovalis, which is a remnant of an opening in the fetal heart known as the foramen ovale.[8] Most of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface has prominent ridges of pectinate muscles, which are also present in the right atrial appendage.[8]

The right atrium is connected to the right ventricle by the tricuspid valve.[8] The walls of the right ventricle are lined with trabeculae carneae, ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the lower part of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle.[8] The right ventricle tapers into the pulmonary trunk, into which it ejects blood when contracting. The pulmonary trunk branches into the left and right pulmonary arteries that carry the blood to each lung. The pulmonary valve lies between the right heart and the pulmonary trunk.[8]

Left heart

The left heart has two chambers: the left atrium and the left ventricle, separated by the mitral valve.[8]

The left atrium receives oxygenated blood back from the lungs via one of the four pulmonary veins. The left atrium has an outpouching called the left atrial appendage. Like the right atrium, the left atrium is lined by pectinate muscles.[25] The left atrium is connected to the left ventricle by the mitral valve.[8]

The left ventricle is much thicker as compared with the right, due to the greater force needed to pump blood to the entire body. Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The left ventricle pumps blood to the body through the aortic valve and into the aorta. Two small openings above the aortic valve carry blood to the heart muscle; the left coronary artery is above the left cusp of the valve, and the right coronary artery is above the right cusp.[8]

Wall

The heart wall is made up of three layers: the inner endocardium, middle myocardium and outer epicardium. These are surrounded by a double-membraned sac called the pericardium.

The innermost layer of the heart is called the endocardium. It is made up of a lining of simple squamous epithelium and covers heart chambers and valves. It is continuous with the endothelium of the veins and arteries of the heart, and is joined to the myocardium with a thin layer of connective tissue.[8] The endocardium, by secreting endothelins, may also play a role in regulating the contraction of the myocardium.[8]

The middle layer of the heart wall is the myocardium, which is the cardiac musclea layer of involuntary striated muscle tissue surrounded by a framework of collagen. The cardiac muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart, with the outer muscles forming a figure 8 pattern around the atria and around the bases of the great vessels and the inner muscles, forming a figure 8 around the two ventricles and proceeding toward the apex. This complex swirling pattern allows the heart to pump blood more effectively.[8]

There are two types of cells in cardiac muscle: muscle cells which have the ability to contract easily, and pacemaker cells of the conducting system. The muscle cells make up the bulk (99%) of cells in the atria and ventricles. These contractile cells are connected by intercalated discs which allow a rapid response to impulses of action potential from the pacemaker cells. The intercalated discs allow the cells to act as a syncytium and enable the contractions that pump blood through the heart and into the major arteries.[8] The pacemaker cells make up 1% of cells and form the conduction system of the heart. They are generally much smaller than the contractile cells and have few myofibrils which gives them limited contractibility. Their function is similar in many respects to neurons.[8] Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed ratespreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart.[8]

There are specific proteins expressed in cardiac muscle cells.[26][27] These are mostly associated with muscle contraction, and bind with actin, myosin, tropomyosin, and troponin. They include MYH6, ACTC1, TNNI3, CDH2 and PKP2. Other proteins expressed are MYH7 and LDB3 that are also expressed in skeletal muscle.[28]

Pericardium

The pericardium is the sac that surrounds the heart. The tough outer surface of the pericardium is called the fibrous membrane. This is lined by a double inner membrane called the serous membrane that produces pericardial fluid to lubricate the surface of the heart. The part of the serous membrane attached to the fibrous membrane is called the parietal pericardium, while the part of the serous membrane attached to the heart is known as the visceral pericardium. The pericardium is present in order to lubricate its movement against other structures within the chest, to keep the heart's position stabilised within the chest, and to protect the heart from infection.[30]

Coronary circulation

Heart tissue, like all cells in the body, needs to be supplied with oxygen, nutrients and a way of removing metabolic wastes. This is achieved by the coronary circulation, which includes arteries, veins, and lymphatic vessels. Blood flow through the coronary vessels occurs in peaks and troughs relating to the heart muscle's relaxation or contraction.[8]

Heart tissue receives blood from two arteries which arise just above the aortic valve. These are the left main coronary artery and the right coronary artery. The left main coronary artery splits shortly after leaving the aorta into two vessels, the left anterior descending and the left circumflex artery. The left anterior descending artery supplies heart tissue and the front, outer side, and septum of the left ventricle. It does this by branching into smaller arteriesdiagonal and septal branches. The left circumflex supplies the back and underneath of the left ventricle. The right coronary artery supplies the right atrium, right ventricle, and lower posterior sections of the left ventricle. The right coronary artery also supplies blood to the atrioventricular node (in about 90% of people) and the sinoatrial node (in about 60% of people). The right coronary artery runs in a groove at the back of the heart and the left anterior descending artery runs in a groove at the front. There is significant variation between people in the anatomy of the arteries that supply the heart. The arteries divide at their furthest reaches into smaller branches that join at the edges of each arterial distribution.[8]

The coronary sinus is a large vein that drains into the right atrium, and receives most of the venous drainage of the heart. It receives blood from the great cardiac vein (receiving the left atrium and both ventricles), the posterior cardiac vein (draining the back of the left ventricle), the middle cardiac vein (draining the bottom of the left and right ventricles), and small cardiac veins. The anterior cardiac veins drain the front of the right ventricle and drain directly into the right atrium.[8]

Small lymphatic networks called plexuses exist beneath each of the three layers of the heart. These networks collect into a main left and a main right trunk, which travel up the groove between the ventricles that exists on the heart's surface, receiving smaller vessels as they travel up. These vessels then travel into the atrioventricular groove, and receive a third vessel which drains the section of the left ventricle sitting on the diaphragm. The left vessel joins with this third vessel, and travels along the pulmonary artery and left atrium, ending in the inferior tracheobronchial node. The right vessel travels along the right atrium and the part of the right ventricle sitting on the diaphragm. It usually then travels in front of the ascending aorta and then ends in a brachiocephalic node.

Nerve supply

The heart receives nerve signals from the vagus nerve and from nerves arising from the sympathetic trunk. These nerves act to influence, but not control, the heart rate. Sympathetic nerves also influence the force of heart contraction. Signals that travel along these nerves arise from two paired cardiovascular centres in the medulla oblongata. The vagus nerve of the parasympathetic nervous system acts to decrease the heart rate, and nerves from the sympathetic trunk act to increase the heart rate.[8] These nerves form a network of nerves that lies over the heart called the cardiac plexus.[8]

The vagus nerve is a long, wandering nerve that emerges from the brainstem and provides parasympathetic stimulation to a large number of organs in the thorax and abdomen, including the heart. The nerves from the sympathetic trunk emerge through the T1T4 thoracic ganglia and travel to both the sinoatrial and atrioventricular nodes, as well as to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves[citation needed]. This shortens the repolarisation period, thus speeding the rate of depolarisation and contraction, which results in an increased heart rate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.[8] Norepinephrine binds to the beta1 receptor.[8]

Development

The heart is the first functional organ to develop and starts to beat and pump blood at about three weeks into embryogenesis. This early start is crucial for subsequent embryonic and prenatal development.

The heart derives from splanchnopleuric mesenchyme in the neural plate which forms the cardiogenic region. Two endocardial tubes form here that fuse to form a primitive heart tube known as the tubular heart.[36] Between the third and fourth week, the heart tube lengthens, and begins to fold to form an S-shape within the pericardium. This places the chambers and major vessels into the correct alignment for the developed heart. Further development will include the formation of the septa and the valves and the remodeling of the heart chambers. By the end of the fifth week, the septa are complete, and by the ninth week, the heart valves are complete.[8]

Before the fifth week, there is an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the lungs. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern. A depression in the surface of the right atrium remains where the foramen ovale was, called the fossa ovalis.[8]

The embryonic heart begins beating at around 22 days after conception (5 weeks after the last normal menstrual period, LMP). It starts to beat at a rate near to the mother's which is about 7580 beats per minute (bpm). The embryonic heart rate then accelerates and reaches a peak rate of 165185 bpm early in the early 7th week (early 9th week after the LMP).[37][38] After 9 weeks (start of the fetal stage) it starts to decelerate, slowing to around 145 (25) bpm at birth. There is no difference in female and male heart rates before birth.[39]

Physiology

Blood flow

The heart functions as a pump in the circulatory system to provide a continuous flow of blood throughout the body. This circulation consists of the systemic circulation to and from the body and the pulmonary circulation to and from the lungs. Blood in the pulmonary circulation exchanges carbon dioxide for oxygen in the lungs through the process of respiration. The systemic circulation then transports oxygen to the body and returns carbon dioxide and relatively deoxygenated blood to the heart for transfer to the lungs.[8]

The right heart collects deoxygenated blood from two large veins, the superior and inferior venae cavae. Blood collects in the right and left atrium continuously.[8] The superior vena cava drains blood from above the diaphragm and empties into the upper back part of the right atrium. The inferior vena cava drains the blood from below the diaphragm and empties into the back part of the atrium below the opening for the superior vena cava. Immediately above and to the middle of the opening of the inferior vena cava is the opening of the thin-walled coronary sinus.[8] Additionally, the coronary sinus returns deoxygenated blood from the myocardium to the right atrium. The blood collects in the right atrium. When the right atrium contracts, the blood is pumped through the tricuspid valve into the right ventricle. As the right ventricle contracts, the tricuspid valve closes and the blood is pumped into the pulmonary trunk through the pulmonary valve. The pulmonary trunk divides into pulmonary arteries and progressively smaller arteries throughout the lungs, until it reaches capillaries. As these pass by alveoli carbon dioxide is exchanged for oxygen. This happens through the passive process of diffusion.

In the left heart, oxygenated blood is returned to the left atrium via the pulmonary veins. It is then pumped into the left ventricle through the mitral valve and into the aorta through the aortic valve for systemic circulation. The aorta is a large artery that branches into many smaller arteries, arterioles, and ultimately capillaries. In the capillaries, oxygen and nutrients from blood are supplied to body cells for metabolism, and exchanged for carbon dioxide and waste products.[8] Capillary blood, now deoxygenated, travels into venules and veins that ultimately collect in the superior and inferior vena cavae, and into the right heart.

Cardiac cycle

The cardiac cycle is the sequence of events in which the heart contracts and relaxes with every heartbeat. The period of time during which the ventricles contract, forcing blood out into the aorta and main pulmonary artery, is known as systole, while the period during which the ventricles relax and refill with blood is known as diastole. The atria and ventricles work in concert, so in systole when the ventricles are contracting, the atria are relaxed and collecting blood. When the ventricles are relaxed in diastole, the atria contract to pump blood to the ventricles. This coordination ensures blood is pumped efficiently to the body.[8]

At the beginning of the cardiac cycle, the ventricles are relaxing. As they do so, they are filled by blood passing through the open mitral and tricuspid valves. After the ventricles have completed most of their filling, the atria contract, forcing further blood into the ventricles and priming the pump. Next, the ventricles start to contract. As the pressure rises within the cavities of the ventricles, the mitral and tricuspid valves are forced shut. As the pressure within the ventricles rises further, exceeding the pressure with the aorta and pulmonary arteries, the aortic and pulmonary valves open. Blood is ejected from the heart, causing the pressure within the ventricles to fall. Simultaneously, the atria refill as blood flows into the right atrium through the superior and inferior vena cavae, and into the left atrium through the pulmonary veins. Finally, when the pressure within the ventricles falls below the pressure within the aorta and pulmonary arteries, the aortic and pulmonary valves close. The ventricles start to relax, the mitral and tricuspid valves open, and the cycle begins again.

Cardiac output

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle (stroke volume) in one minute. This is calculated by multiplying the stroke volume (SV) by the beats per minute of the heart rate (HR). So that: CO = SV x HR.[8]The cardiac output is normalized to body size through body surface area and is called the cardiac index.

The average cardiac output, using an average stroke volume of about 70mL, is 5.25 L/min, with a normal range of 4.08.0 L/min.[8] The stroke volume is normally measured using an echocardiogram and can be influenced by the size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload and afterload.[8]

Preload refers to the filling pressure of the atria at the end of diastole, when the ventricles are at their fullest. A main factor is how long it takes the ventricles to fill: if the ventricles contract more frequently, then there is less time to fill and the preload will be less.[8] Preload can also be affected by a person's blood volume. The force of each contraction of the heart muscle is proportional to the preload, described as the Frank-Starling mechanism. This states that the force of contraction is directly proportional to the initial length of muscle fiber, meaning a ventricle will contract more forcefully, the more it is stretched.[8]

Afterload, or how much pressure the heart must generate to eject blood at systole, is influenced by vascular resistance. It can be influenced by narrowing of the heart valves (stenosis) or contraction or relaxation of the peripheral blood vessels.[8]

The strength of heart muscle contractions controls the stroke volume. This can be influenced positively or negatively by agents termed inotropes.[41] These agents can be a result of changes within the body, or be given as drugs as part of treatment for a medical disorder, or as a form of life support, particularly in intensive care units. Inotropes that increase the force of contraction are "positive" inotropes, and include sympathetic agents such as adrenaline, noradrenaline and dopamine.[42] "Negative" inotropes decrease the force of contraction and include calcium channel blockers.[41]

Electrical conduction

The normal rhythmical heart beat, called sinus rhythm, is established by the heart's own pacemaker, the sinoatrial node (also known as the sinus node or the SA node). Here an electrical signal is created that travels through the heart, causing the heart muscle to contract. The sinoatrial node is found in the upper part of the right atrium near to the junction with the superior vena cava.[43] The electrical signal generated by the sinoatrial node travels through the right atrium in a radial way that is not completely understood. It travels to the left atrium via Bachmann's bundle, such that the muscles of the left and right atria contract together.[44][45][46] The signal then travels to the atrioventricular node. This is found at the bottom of the right atrium in the atrioventricular septum, the boundary between the right atrium and the left ventricle. The septum is part of the cardiac skeleton, tissue within the heart that the electrical signal cannot pass through, which forces the signal to pass through the atrioventricular node only.[8] The signal then travels along the bundle of His to left and right bundle branches through to the ventricles of the heart. In the ventricles the signal is carried by specialized tissue called the Purkinje fibers which then transmit the electric charge to the heart muscle.[47]

Heart rate

Heart sounds of a 16 year old girl immediately after running, with a heart rate of 186 BPM.

The normal resting heart rate is called the sinus rhythm, created and sustained by the sinoatrial node, a group of pacemaking cells found in the wall of the right atrium. Cells in the sinoatrial node do this by creating an action potential. The cardiac action potential is created by the movement of specific electrolytes into and out of the pacemaker cells. The action potential then spreads to nearby cells.

When the sinoatrial cells are resting, they have a negative charge on their membranes. A rapid influx of sodium ions causes the membrane's charge to become positive; this is called depolarisation and occurs spontaneously.[8] Once the cell has a sufficiently high charge, the sodium channels close and calcium ions then begin to enter the cell, shortly after which potassium begins to leave it. All the ions travel through ion channels in the membrane of the sinoatrial cells. The potassium and calcium start to move out of and into the cell only once it has a sufficiently high charge, and so are called voltage-gated. Shortly after this, the calcium channels close and potassium channels open, allowing potassium to leave the cell. This causes the cell to have a negative resting charge and is called repolarisation. When the membrane potential reaches approximately 60 mV, the potassium channels close and the process may begin again.[8]

The ions move from areas where they are concentrated to where they are not. For this reason sodium moves into the cell from outside, and potassium moves from within the cell to outside the cell. Calcium also plays a critical role. Their influx through slow channels means that the sinoatrial cells have a prolonged "plateau" phase when they have a positive charge. A part of this is called the absolute refractory period. Calcium ions also combine with the regulatory protein troponin C in the troponin complex to enable contraction of the cardiac muscle, and separate from the protein to allow relaxation.[49]

The adult resting heart rate ranges from 60 to 100 bpm. The resting heart rate of a newborn can be 129 beats per minute (bpm) and this gradually decreases until maturity.[50] An athlete's heart rate can be lower than 60 bpm. During exercise the rate can be 150 bpm with maximum rates reaching from 200 to 220 bpm.[8]

Influences

The normal sinus rhythm of the heart, giving the resting heart rate, is influenced by a number of factors. The cardiovascular centres in the brainstem control the sympathetic and parasympathetic influences to the heart through the vagus nerve and sympathetic trunk.[51] These cardiovascular centres receive input from a series of receptors including baroreceptors, sensing the stretching of blood vessels and chemoreceptors, sensing the amount of oxygen and carbon dioxide in the blood and its pH. Through a series of reflexes these help regulate and sustain blood flow.[8]

Baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Baroreceptors fire at a rate determined by how much they are stretched, which is influenced by blood pressure, level of physical activity, and the relative distribution of blood. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.[8] There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase heart rate. The opposite is also true.[8] Chemoreceptors present in the carotid body or adjacent to the aorta in an aortic body respond to the blood's oxygen, carbon dioxide levels. Low oxygen or high carbon dioxide will stimulate firing of the receptors.

Exercise and fitness levels, age, body temperature, basal metabolic rate, and even a person's emotional state can all affect the heart rate. High levels of the hormones epinephrine, norepinephrine, and thyroid hormones can increase the heart rate. The levels of electrolytes including calcium, potassium, and sodium can also influence the speed and regularity of the heart rate; low blood oxygen, low blood pressure and dehydration may increase it.[8]

Clinical significance

Diseases

Cardiovascular diseases, which include diseases of the heart, are the leading cause of death worldwide.[54] The majority of cardiovascular disease is noncommunicable and related to lifestyle and other factors, becoming more prevalent with ageing.[54] Heart disease is a major cause of death, accounting for an average of 30% of all deaths in 2008, globally.[12] This rate varies from a lower 28% to a high 40% in high-income countries.[13] Doctors that specialise in the heart are called cardiologists. Many other medical professionals are involved in treating diseases of the heart, including doctors, cardiothoracic surgeons, intensivists, and allied health practitioners including physiotherapists and dieticians.[55]

Ischemic heart disease

Coronary artery disease, also known as ischemic heart disease, is caused by atherosclerosisa build-up of fatty material along the inner walls of the arteries. These fatty deposits known as atherosclerotic plaques narrow the coronary arteries, and if severe may reduce blood flow to the heart.[56] If a narrowing (or stenosis) is relatively minor then the patient may not experience any symptoms. Severe narrowings may cause chest pain (angina) or breathlessness during exercise or even at rest. The thin covering of an atherosclerotic plaque can rupture, exposing the fatty centre to the circulating blood. In this case a clot or thrombus can form, blocking the artery, and restricting blood flow to an area of heart muscle causing a myocardial infarction (a heart attack) or unstable angina. In the worst case this may cause cardiac arrest, a sudden and utter loss of output from the heart. Obesity, high blood pressure, uncontrolled diabetes, smoking and high cholesterol can all increase the risk of developing atherosclerosis and coronary artery disease.[54][56]

Heart failure

Heart failure is defined as a condition in which the heart is unable to pump enough blood to meet the demands of the body.[59] Patients with heart failure may experience breathlessness especially when lying flat, as well as ankle swelling, known as peripheral oedema. Heart failure is the result of many diseases affecting the heart, but is most commonly associated with ischemic heart disease, valvular heart disease, or high blood pressure. Less common causes include various cardiomyopathies. Heart failure is frequently associated with weakness of the heart muscle in the ventricles (systolic heart failure), but can also be seen in patients with heart muscle that is strong but stiff (diastolic heart failure). The condition may affect the left ventricle (causing predominantly breathlessness), the right ventricle (causing predominantly swelling of the legs and an elevated jugular venous pressure), or both ventricles. Patients with heart failure are at higher risk of developing dangerous heart rhythm disturbances or arrhythmias.[59]

Cardiomyopathies

Cardiomyopathies are diseases affecting the muscle of the heart. Some cause abnormal thickening of the heart muscle (hypertrophic cardiomyopathy), some cause the heart to abnormally expand and weaken (dilated cardiomyopathy), some cause the heart muscle to become stiff and unable to fully relax between contractions (restrictive cardiomyopathy) and some make the heart prone to abnormal heart rhythms (arrhythmogenic cardiomyopathy). These conditions are often genetic and can be inherited, but some such as dilated cardiomyopathy may be caused by damage from toxins such as alcohol. Some cardiomyopathies such as hypertrophic cardiomopathy are linked to a higher risk of sudden cardiac death, particularly in athletes.[8] Many cardiomyopathies can lead to heart failure in the later stages of the disease.[59]

Valvular heart disease

Heart sounds of a 16 year old girl diagnosed with mitral valve prolapse and mitral regurgitation. Auscultating her heart, a systolic murmur and click is heard. Recorded with the stethoscope over the mitral valve.

Healthy heart valves allow blood to flow easily in one direction, and prevent it from flowing in the other direction. A diseased heart valve may have a narrow opening (stenosis), that restricts the flow of blood in the forward direction. A valve may otherwise be leaky, allowing blood to leak in the reverse direction (regurgitation). Valvular heart disease may cause breathlessness, blackouts, or chest pain, but may be asymptomatic and only detected on a routine examination by hearing abnormal heart sounds or a heart murmur. In the developed world, valvular heart disease is most commonly caused by degeneration secondary to old age, but may also be caused by infection of the heart valves (endocarditis). In some parts of the world rheumatic heart disease is a major cause of valvular heart disease, typically leading to mitral or aortic stenosis and caused by the body's immune system reacting to a streptococcal throat infection.[60]

Cardiac arrhythmias

While in the healthy heart, waves of electrical impulses originate in the sinus node before spreading to the rest of the atria, the atrioventricular node, and finally the ventricles (referred to as a normal sinus rhythm), this normal rhythm can be disrupted. Abnormal heart rhythms or arrhythmias may be asymptomatic or may cause palpitations, blackouts, or breathlessness. Some types of arrhythmia such as atrial fibrillation increase the long term risk of stroke.[62]

Some arrhythmias cause the heart to beat abnormally slowly, referred to as a bradycardia or bradyarrhythmia. This may be caused by an abnormally slow sinus node or damage within the cardiac conduction system (heart block).[63] In other arrhythmias the heart may beat abnormally rapidly, referred to as a tachycardia or tachyarrhythmia. These arrhythmias can take many forms and can originate from different structures within the heartsome arise from the atria (e.g. atrial flutter), some from the atrioventricular node (e.g. AV nodal re-entrant tachycardia) whilst others arise from the ventricles (e.g. ventricular tachycardia). Some tachyarrhythmias are caused by scarring within the heart (e.g. some forms of ventricular tachycardia), others by an irritable focus (e.g. focal atrial tachycardia), while others are caused by additional abnormal conduction tissue that has been present since birth (e.g. Wolff-Parkinson-White syndrome). The most dangerous form of heart racing is ventricular fibrillation, in which the ventricles quiver rather than contract, and which if untreated is rapidly fatal.[64]

Pericardial disease

The sac which surrounds the heart, called the pericardium, can become inflamed in a condition known as pericarditis. This condition typically causes chest pain that may spread to the back, and is often caused by a viral infection (glandular fever, cytomegalovirus, or coxsackievirus). Fluid can build up within the pericardial sac, referred to as a pericardial effusion. Pericardial effusions often occur secondary to pericarditis, kidney failure, or tumours, and frequently do not cause any symptoms. However, large effusions or effusions which accumulate rapidly can compress the heart in a condition known as cardiac tamponade, causing breathlessness and potentially fatal low blood pressure. Fluid can be removed from the pericardial space for diagnosis or to relieve tamponade using a syringe in a procedure called pericardiocentesis.

Congenital heart disease

Some people are born with hearts that are abnormal and these abnormalities are known as congenital heart defects. They may range from the relatively minor (e.g. patent foramen ovale, arguably a variant of normal) to serious life-threatening abnormalities (e.g. hypoplastic left heart syndrome). Common abnormalities include those that affect the heart muscle that separates the two side of the heart (a "hole in the heart", e.g. ventricular septal defect). Other defects include those affecting the heart valves (e.g. congenital aortic stenosis), or the main blood vessels that lead from the heart (e.g. coarctation of the aorta). More complex syndromes are seen that affect more than one part of the heart (e.g. Tetralogy of Fallot).

Some congenital heart defects allow blood that is low in oxygen that would normally be returned to the lungs to instead be pumped back to the rest of the body. These are known as cyanotic congenital heart defects and are often more serious. Major congenital heart defects are often picked up in childhood, shortly after birth, or even before a child is born (e.g. transposition of the great arteries), causing breathlessness and a lower rate of growth. More minor forms of congenital heart disease may remain undetected for many years and only reveal themselves in adult life (e.g., atrial septal defect).[66]

Channelopathies

Channelopathies can be categorized based on the organ system they affect. In the cardiovascular system, the electrical impulse required for each heart beat is provided by the electrochemical gradient of each heart cell. Because the beating of the heart depends on the proper movement of ions across the surface membrane, cardiac ion channelopathies form a major group of heart diseases.[68][69] Cardiac ion channelopathies may explain some of the cases of sudden death syndrome and sudden arrhythmic death syndrome.[70] Long QT syndrome is the most common form of cardiac channelopathy.

Diagnosis

Heart disease is diagnosed by the taking of a medical history, a cardiac examination, and further investigations, including blood tests, echocardiograms, electrocardiograms, and imaging. Other invasive procedures such as cardiac catheterisation can also play a role.

Examination

The cardiac examination includes inspection, feeling the chest with the hands (palpation) and listening with a stethoscope (auscultation).[77] It involves assessment of signs that may be visible on a person's hands (such as splinter haemorrhages), joints and other areas. A person's pulse is taken, usually at the radial artery near the wrist, in order to assess for the rhythm and strength of the pulse. The blood pressure is taken, using either a manual or automatic sphygmomanometer or using a more invasive measurement from within the artery. Any elevation of the jugular venous pulse is noted. A person's chest is felt for any transmitted vibrations from the heart, and then listened to with a stethoscope.

Heart sounds

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Stephen Kopecky, M.D., Cardiovascular Disease, Mayo Clinic: I'm Dr. Stephen Kopecky, a cardiologist at Mayo Clinic. In this video, we'll cover the basics of coronary artery disease. What is it? Who gets it? The symptoms, diagnosis and treatment. Whether you're looking for answers for yourself or someone you love, we're here to give you the best information available.

Coronary artery disease, also called CAD, is a condition that affects your heart. It is the most common heart disease in the United States. CAD happens when coronary arteries struggle to supply the heart with enough blood, oxygen and nutrients. Cholesterol deposits, or plaques, are almost always to blame. These buildups narrow your arteries, decreasing blood flow to your heart. This can cause chest pain, shortness of breath or even a heart attack. CAD typically takes a long time to develop. So often, patients don't know that they have it until there's a problem. But there are ways to prevent coronary artery disease, and ways to know if you're at risk and ways to treat it.

Anyone can develop CAD. It begins when fats, cholesterols and other substances gather along the walls of your arteries. This process is called atherosclerosis. It's typically no cause for concern. However, too much buildup can lead to a blockage, obstructing blood flow. There are a number of risk factors, common red flags, that can contribute to this and ultimately lead to coronary artery disease. First, getting older can mean more damaged and narrowed arteries. Second, men are generally at a greater risk. But the risk for women increases after menopause. Existing health conditions matter, too. High blood pressure can thicken your arteries, narrowing your blood flow. High cholesterol levels can increase the rate of plaque buildup. Diabetes is also associated with higher risk, as is being overweight. Your lifestyle plays a large role as well. Physical inactivity, long periods of unrelieved stress in your life, an unhealthy diet and smoking can all increase your risk. And finally, family history. If a close relative was diagnosed at an early age with heart disease, you're at a greater risk. All these factors together can paint a picture of your risk for developing CAD.

When coronary arteries become narrow, the heart doesn't get enough oxygen-rich blood. Remember, unlike most pumps, the heart has to pump its own energy supply. It's working harder with less. And you may begin to notice these signs and symptoms of pressure or tightness in your chest. This pain is called angina. It may feel like somebody is standing on your chest. When your heart can't pump enough blood to meet your body's needs, you might develop shortness of breath or extreme fatigue during activities. And if an artery becomes totally blocked, it leads to a heart attack. Classic signs and symptoms of a heart attack include crushing, substernal chest pain, pain in your shoulders or arms, shortness of breath, and sweating. However, many heart attacks have minimal or no symptoms and are found later during routine testing.

Diagnosing CAD starts by talking to your doctor. They'll be able to look at your medical history, do a physical exam and order routine blood work. Depending on that, they may suggest one or more of the following tests: an electrocardiogram or ECG, an echocardiogram or soundwave test of the heart, stress test, cardiac catheterization and angiogram, or a cardiac CT scan.

Treating coronary artery disease usually means making changes to your lifestyle. This might be eating healthier foods, exercising regularly, losing excess weight, reducing stress or quitting smoking. The good news is these changes can do a lot to improve your outlook. Living a healthier life translates to having healthier arteries. When necessary, treatment could involve drugs like aspirin, cholesterol-modifying medications, beta-blockers, or certain medical procedures like angioplasty or coronary artery bypass surgery.

Discovering you have coronary artery disease can be overwhelming. But be encouraged. There are things you can do to manage and live with this condition. Reducing cholesterol, lowering blood pressure, quitting tobacco, eating healthier, exercising and managing your stress can make a world of difference. Better heart health starts by educating yourself. So don't be afraid to seek out information and ask your doctors about coronary artery disease. If you'd like to learn even more about this condition, watch our other related videos or visit Mayoclinic.org. We wish you well.

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1

: of, relating to, situated near, or acting on the heart

2

: a person with heart disease

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CARDIAC Definition & Meaning - Merriam-Webster

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heart, organ that serves as a pump to circulate the blood. It may be a straight tube, as in spiders and annelid worms, or a somewhat more elaborate structure with one or more receiving chambers (atria) and a main pumping chamber (ventricle), as in mollusks. In fishes the heart is a folded tube, with three or four enlarged areas that correspond to the chambers in the mammalian heart. In animals with lungsamphibians, reptiles, birds, and mammalsthe heart shows various stages of evolution from a single to a double pump that circulates blood (1) to the lungs and (2) to the body as a whole.

In humans and other mammals and in birds, the heart is a four-chambered double pump that is the centre of the circulatory system. In humans it is situated between the two lungs and slightly to the left of centre, behind the breastbone; it rests on the diaphragm, the muscular partition between the chest and the abdominal cavity.

The heart consists of several layers of a tough muscular wall, the myocardium. A thin layer of tissue, the pericardium, covers the outside, and another layer, the endocardium, lines the inside. The heart cavity is divided down the middle into a right and a left heart, which in turn are subdivided into two chambers. The upper chamber is called an atrium (or auricle), and the lower chamber is called a ventricle. The two atria act as receiving chambers for blood entering the heart; the more muscular ventricles pump the blood out of the heart.

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The heart, although a single organ, can be considered as two pumps that propel blood through two different circuits. The right atrium receives venous blood from the head, chest, and arms via the large vein called the superior vena cava and receives blood from the abdomen, pelvic region, and legs via the inferior vena cava. Blood then passes through the tricuspid valve to the right ventricle, which propels it through the pulmonary artery to the lungs. In the lungs venous blood comes in contact with inhaled air, picks up oxygen, and loses carbon dioxide. Oxygenated blood is returned to the left atrium through the pulmonary veins. Valves in the heart allow blood to flow in one direction only and help maintain the pressure required to pump the blood.

The low-pressure circuit from the heart (right atrium and right ventricle), through the lungs, and back to the heart (left atrium) constitutes the pulmonary circulation. Passage of blood through the left atrium, bicuspid valve, left ventricle, aorta, tissues of the body, and back to the right atrium constitutes the systemic circulation. Blood pressure is greatest in the left ventricle and in the aorta and its arterial branches. Pressure is reduced in the capillaries (vessels of minute diameter) and is reduced further in the veins returning blood to the right atrium.

The pumping of the heart, or the heartbeat, is caused by alternating contractions and relaxations of the myocardium. These contractions are stimulated by electrical impulses from a natural pacemaker, the sinoatrial, or S-A, node located in the muscle of the right atrium. An impulse from the S-A node causes the two atria to contract, forcing blood into the ventricles. Contraction of the ventricles is controlled by impulses from the atrioventricular, or A-V, node located at the junction of the two atria. Following contraction, the ventricles relax, and pressure within them falls. Blood again flows into the atria, and an impulse from the S-A starts the cycle over again. This process is called the cardiac cycle. The period of relaxation is called diastole. The period of contraction is called systole. Diastole is the longer of the two phases so that the heart can rest between contractions. In general, the rate of heartbeat varies inversely with the size of the animal. In elephants it averages 25 beats per minute, in canaries about 1,000. In humans the rate diminishes progressively from birth (when it averages 130) to adolescence but increases slightly in old age; the average adult rate is 70 beats at rest. The rate increases temporarily during exercise, emotional excitement, and fever and decreases during sleep. Rhythmic pulsation felt on the chest, coinciding with heartbeat, is called the apex beat. It is caused by pressure exerted on the chest wall at the outset of systole by the rounded and hardened ventricular wall.

The rhythmic noises accompanying heartbeat are called heart sounds. Normally, two distinct sounds are heard through the stethoscope: a low, slightly prolonged lub (first sound) occurring at the beginning of ventricular contraction, or systole, and produced by closure of the mitral and tricuspid valves, and a sharper, higher-pitched dup (second sound), caused by closure of aortic and pulmonary valves at the end of systole. Occasionally audible in normal hearts is a third soft, low-pitched sound coinciding with early diastole and thought to be produced by vibrations of the ventricular wall. A fourth sound, also occurring during diastole, is revealed by graphic methods but is usually inaudible in normal subjects; it is believed to be the result of atrial contraction and the impact of blood, expelled from the atria, against the ventricular wall.

Heart murmurs may be readily heard by a physician as soft swishing or hissing sounds that follow the normal sounds of heart action. Murmurs may indicate that blood is leaking through an imperfectly closed valve and may signal the presence of a serious heart problem. Coronary heart disease, in which an inadequate supply of oxygen-rich blood is delivered to the myocardium owing to the narrowing or blockage of a coronary artery by fatty plaques, is a leading cause of death worldwide.

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Heart | Structure, Function, Diagram, Anatomy, & Facts | Britannica

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