Dilated Cardiomyopathy Essay

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

ATP is required to break the attachment of actin to the myosin head. At death, calcium ions leak out of the SR

Cytoplasmic streaming is the organised flow of the cytoplasm and its constituents within a living cell (Shimmen et al., 2004). Organelles and important molecules move through the cytosol along the structure of the cytoskeleton (actin filaments and microtubules) with the aid of myosin I, an actin-binding motor protein that plays a part in various cell functions including cell motility and endocytosis (Flavell et al., 2008). Actin microfilaments (F-actin) are the thinnest filaments of the cytoskeleton,

In systolic ventricular dysfunction or systolic heart failure the heart is not able to produce enough output for adequate tissue perfusion. Heart rate and stroke volume produce cardiac output. Contractility, preload, and afterload influence the heart’s stroke volume. These factors are important in understanding the pathophysiologic consequences of this syndrome and possible treatments. Patients with systolic heart failure usually have dilated, large ventricles and impaired systolic function.

Muscle fibres, as shown in Diagram 1, consist of myofibrils, which contain the proteins, actin and myosin, in specific arrangements . The diagram illustrates how a muscle is made up of many fascicles, which in turn are made up of many endomysiums, and within them, many muscle fibres. Each muscle fibre is made up of many myofibrils that consist of sarcomeres bound end on end . Actin is a thin filament, about 7nm in diameter, and myosin is a thick filament, about 15nm in diameter , both of which reside in the sarcomere. They are held together by transverse bands known as Z lines . Diagram 2 shows actin and myosin filaments within a sarcomere, and the Z lines that connect them.

Myofibrils are made up of long proteins that include myosin, titin, and actin while other proteins bind them together. These proteins are arranged into thin and thick filaments that are repetitive along the myofibril in sectors known as sarcomeres. The sliding of actin and myosin filaments along each other is when the muscle is contracting. Dark A-bands and light I-bands reappear along myofibrils. The alignment of myofibrils causes an appearance of the cell to look banded or striated. A myofibril is made up of lots of sarcomeres. As the sarcomeres contract individually the muscle cells and myofibrils shorten in length. The longitudinal section of skeletal muscle exhibits a unique pattern of alternating light and dark bands. The dark staining, A-bands possess a pale region in the middle called the H-zone. In the middle of the H-zone the M-line is found, that displays filamentous structures that can join the thick filaments. The light-staining bands also known as I-bands are divided by thin Z-line. These striated patterns appear because of the presence of myofibrils in the sarcoplasm (IUPUI, 2016).

When a muscle contracts, myosin heads in thick filaments bind to actin in thin filaments and pulls the thin filament, shortening the length of the muscle fiber. However, without Ca++ when troponin binds to actin, the tropomyosin moves into a position that

Pasternak C, Wong S, Elson EL. (1995). Mechanical function of dystrophin in muscle cells. The Journal of Cell Biology, 128(3), 355-361. doi:10.1083/jcb.128.3.355

Actin and myosin filaments can be found in skeletal muscle and are the smallest units that form a sarcomere, which is the smallest contractile unit in muscle (Baechle, 2008). The Sliding Filament Theory states that the actin filaments slide inward on the myosin filaments, pulling on the boundaries of the sarcomere, causing it to shorten the muscle fiber, also known as a concentric muscular contraction (Baechle, 2008). The Sliding Filament Theory is composed of five steps: the “Resting Phase”, the “Excitation-Contraction Coupling Phase”, the “Contraction Phase”, the “Recharge Phase”, and the “Relaxation Phase” (Baechle, 2008). During the Resting Phase, the actin and myosin filaments are lined up with no cross-bridge binding of the two filaments. During the Excitation-Contraction Coupling Phase, Calcium is released from the sarcoplasmic reticulum and binds to troponin, causing a shift in tropomyosin where the binding cites are exposed (Baechle, 2008). When the binding cites are exposed, the myosin cross-bridge head attaches to actin. During the Contraction Phase, ATP bonds break, releasing energy that is used to allow the myosin head to flex, causing the actin filaments to move toward the M-bridge. During the Recharge Phase, there is a continuous repetition of the Excitation-Contraction Coupling Phase and the Contraction Phase in order to produce muscular

Dilated cardiomyopathy is thought to have many different causes. Some of the causes are thought to be: “Genetic conditions, long-term high blood pressure, heart tissue damage from a previous heart attack, chronic rapid heart rate, drinking too much alcohol over the years and certain infection” (Mayo Clinic Staff, 2015). Cardiomyopathy has been seen in a wide range of individuals; there is no clear age distinction and may be passed on genetically or not.

Calcium ions exposes the binding sites on the actin filaments. Calcium ions binds to the troponin molecule causing tropomyosin to expose positions on the actin filament for the attachment of myosin heads. Cross bridges between myosin heads and actin filaments form. When attachment sites on the actin are exposed, the myosin heads bind to actin to form cross bridges. ADP and Pi are released, and sliding motion of actin results.

actin “slid” past each other and neither filament changed in length. In 1957 Allan Huxley

form of myosin ATP and are not very good at delivering calcium to the muscle

Immunohistochemical analysis for smooth muscle actin (SMA) was done and the intensity of staining and staining location were considered.