Hypertrophy

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Hypertrophy
Hyperplasia vs Hypertrophy.svg
Hypertrophy results from an increase in cell size, whereas hyperplasia stems from an increase in cell number.

Hypertrophy is the increase in the volume of an organ or tissue due to the enlargement of its component cells. [1] It is distinguished from hyperplasia, in which the cells remain approximately the same size but increase in number. [2] Although hypertrophy and hyperplasia are two distinct processes, they frequently occur together, such as in the case of the hormonally induced proliferation and enlargement of the cells of the uterus during pregnancy.

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Eccentric hypertrophy is a type of hypertrophy where the walls and chamber of a hollow organ undergo growth in which the overall size and volume are enlarged. It is applied especially to the left ventricle of heart. [3] Sarcomeres are added in series, as for example in dilated cardiomyopathy (in contrast to hypertrophic cardiomyopathy, a type of concentric hypertrophy, where sarcomeres are added in parallel).

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Cardiac muscle is one of three types of vertebrate muscle tissues, with the other two being skeletal muscle and smooth muscle. It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart. The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall and the inner layer, with blood supplied via the coronary circulation. It is composed of individual cardiac muscle cells joined by intercalated discs, and encased by collagen fibers and other substances that form the extracellular matrix.

<span class="mw-page-title-main">Frank–Starling law</span> Relationship between stroke volume and end diastolic volume

The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

<span class="mw-page-title-main">Striated muscle tissue</span> Muscle tissue with repeating functional units called sarcomeres

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Hypertrophic cardiomyopathy is a condition in which muscle tissues of the heart become thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems.

<span class="mw-page-title-main">Left ventricular hypertrophy</span> Medical condition

Left ventricular hypertrophy (LVH) is thickening of the heart muscle of the left ventricle of the heart, that is, left-sided ventricular hypertrophy and resulting increased left ventricular mass.

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Ventricular hypertrophy (VH) is thickening of the walls of a ventricle of the heart. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur.

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Right ventricular hypertrophy (RVH) is a condition defined by an abnormal enlargement of the cardiac muscle surrounding the right ventricle. The right ventricle is one of the four chambers of the heart. It is located towards the lower-end of the heart and it receives blood from the right atrium and pumps blood into the lungs.

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The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

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Diabetic cardiomyopathy is a disorder of the heart muscle in people with diabetes. It can lead to inability of the heart to circulate blood through the body effectively, a state known as heart failure(HF), with accumulation of fluid in the lungs or legs. Most heart failure in people with diabetes results from coronary artery disease, and diabetic cardiomyopathy is only said to exist if there is no coronary artery disease to explain the heart muscle disorder.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

Concentric hypertrophy is a hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ are thickened and its capacity or volume is diminished.

Heart problems are more common in people with HIV/AIDS. Those with left ventricular dysfunction have a median survival of 101 days as compared to 472 days in people with AIDS with healthy hearts. HIV is a major cause of cardiomyopathy. The most common type of HIV induced cardiomyopathy is dilated cardiomyopathy also known as eccentric ventricular hypertrophy which leads to impaired contraction of the ventricles due to volume overload. The annual incidence of HIV associated dilated cardiomyopathy was 15.9/1000 before the introduction of highly active antiretroviral therapy (HAART). However, in 2014, a study found that 17.6% of HIV patients have dilated cardiomyopathy (176/1000) meaning the incidence has greatly increased.

References

  1. Hernandez, Richard; Kravitz, Len. "Skeletal muscle hypertrophy". www.unm.edu.
  2. "Hyperplasia: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 2023-02-19.
  3. Kusumoto, F. M. (2004), Cardiovascular Pathophysiology, Hayes Barton Press, pp. 20–22, ISBN   978-1-59377-189-8