Where is the myocardium thicker

What is the treatment for ventricular hypertrophy? What needs to be considered during treatment? Ventricular hypertrophy can have various causes. The most common causes are:. While an increase in cardiac muscle mass from competitive sports is often welcomed, ventricular hypertrophy as a result of increased ventricular pressure or volume load is problematic, and actually poses a serious health risk which can even lead to heart failure.

It is the left ventricle that is most commonly affected, less so the right ventricle. The hereditary form of ventricular hypertrophy, which is usually not caused by pressure overload, is, however, quite rare. As the wall thickness of the left ventricle increases, it becomes stiffer, leading to reduced elasticity so-called diastolic dysfunction.

The first symptoms of a pathological thickening of the heart wall are usually reduced performance or shortness of breath, especially during strenuous physical exertion.

Other symptoms can include the need for frequent urination, chronic fatigue and swollen legs edema. During reperfusion, a continuous decrease in EF was observed.

ED cavity size, as measured by M-mode echocardiography, fell immediately on reperfusion with no further changes occurring over the reperfusion period. Temporal evolution of the left ventricular ejection fraction solid lines; diamonds and the left ventricular end-diastolic cavity size dashed lines; dots. Thick lines represent the statistical models that best described the data while the thin horizontal lines show the baseline value. TTC staining showed the myocardial segments under investigation to be transmurally infarcted in all animals.

Under a magnification of the capillaries appeared intact with no thrombotic plugging. There was neither evidence of blood extravasation or haemorrhage nor any confluent necrosis in either of the specimens examined. The corresponding samples from the non-ischemic anterior and septal walls contained only normal myocardium. TTC stained slice of the infarcted heart middle panel ; dark grey represents normal, viable tissue; light grey shows infarcted tissue.

Microscopic image of the histologic samples of an infarcted, posterior wall segment left and a normal, anterior wall segment right using a magnification of ; asterisks indicate oedema, arrows intact capillaries. Either transient or chronic regional myocardial ischemia is known to induce predictable alterations in local myocardial deformation.

In fact, for this reason, we had chosen to use the circumflex rather than the left anterior descending coronary artery for balloon occlusion. The mechanisms underlying the phenomenon of ischemia-related post-systolic deformation have been the subject of much debate. Three different explanations have been proposed namely either delayed active contraction, late passive thickening or elastic recoil overshoot after bulging.

Thus, the elastic recoil theory could not be applied. Our findings thus suggest that in this animal model the late passive thickening theory is the correct one. This would be in concordance with the observed regional differences in end-systolic wall thickness Fig.

Indeed, if local differences in end-systolic myocardial wall thickness did not change during the ischemic period, interacting forces attempting to thicken the ischemic and thinner myocardium after aortic valve closure, would remain constant given a constant elasticity of the normally perfused myocardium. However, as this constant interaction force resulted in a systematic reduction of the deformation response, local resistance to deformation, i.

Such an increase in myocardial stiffness with ischemia has previously been described. Prior investigators have shown that the induction of post-systolic deformation may serve as a sensitive and early marker of the presence of acute or chronic ischemia.

In itself, the presence of post-systolic deformation in these substrates can thus not be used as a marker of viability but it should be combined with other functional indices. End-systolic strain and peak systolic strain rate and their responses to a stress test could be useful parameters in this context. With TIMI 3 infarct reperfusion, end-systolic posterior wall thickness returned to baseline within 5 min while end-diastolic wall thickness increased above baseline levels after 1 min.

Both wall thickness parameters then continued to increase logarithmically during the 60 min reperfusion period. The corresponding parameters in the non-ischemic septum were not altered by reperfusion. The observed immediate increase in end-diastolic and end-systolic wall thickness with reperfusion can most probably be explained by a combination of immediate reflow and consequent reactive hyperaemia after the opening of the occluded vessel.

Prior histology studies have shown that reperfusion injury is associated with tissue oedema, myocyte damage, micro-vascular and endothelial injury and cell necrosis. Our own histological observations confirmed the consistent finding of marked areas of extravascular tissue oedema separating blocks of myofibrils. However, in this acute model there were no changes of endothelial injury or capillary plugging by thrombosis and platelets. This could be due to either to our methods used in post-mortem preparation of the myocardium in which intra-vascular thrombi might have been washed out by the high-pressure formalin infusion or to the absence of thrombus microemboli which may occur following a clinical PTCA.

We also did not detect either extravasation of blood or haemorrhage in the histologic specimens. This is most likely due to the increased pressure in the tissue caused by the oedema which probably occluded the capillaries and the micro-vasculature. Surrounding tissue was thus most likely compressed causing capillary compression which in turn may have resulted in reduced flow and ischemia leading to infarct extension in the surrounding tissue.

The infarct could thus expand to adjacent segments which were initially not compromised. Neither end-systolic nor post-systolic strain changed significantly during reperfusion. However, as explained above, any remaining post-systolic thickening of infarcted myocardium should be attributed to passive deformation by adjacent, thicker myocardium.

As the end-systolic thickness of the reperfused, infarcted myocardium returned to baseline values, regional differences in wall thickness would thus disappear. The observed, continued post-systolic thickening after reperfusion can thus only be explained by hyper-contractile function of adjacent myocardial segments due to hyperaemia. If reproducible in a clinical population, the measurements of end-diastolic wall thickness might provide a new non-invasive approach to monitoring successful reperfusion therapy and the results of strategies to modify reperfusion injury in patients.

Identical changes in regional wall thickness and deformation have already been observed by the authors in pilot echocardiographic and magnetic resonance studies in patients with successful infarct reperfusion following PTCA.

In this study, we attempted to produce an experimental model, which would closely reproduce the clinical situation of acute coronary artery occlusion in which the supplying vessel was non-flow limiting before the acute occlusion and the distal myocardium was neither chronically ischemic nor stunned.

It was not our intention to model acute occlusion in which the supplying coronary artery had a flow limiting stenosis. Thus our model was potentially representative of only one subset of the clinical population. Also flow restoration in the clinical situation is seldom so acute or total unless effected by primary angioplasty with stent placement. Usually there is reduced reperfusion flow at low pressure. This high reperfusion flow pressure could have been responsible for the absence of any thrombi and platelet plugs in the previously non-perfused capillaries as was found in our histology.

The lack of visual evidence of any cell necrosis in our histologic samples was most likely due to the short time period after infarction 60 min that the hearts were removed. Following an infarction, histologic evidence of cell necrosis usually takes at least 10 h to develop.

In addition, to understand the full range of changes in regional deformation associated with reperfusion injury future experimental studies will have to be carried out in which the distal myocardial substrate has been chronically ischemic for some weeks and post-infarct reperfusion injury is studied in the setting of either non-flow limited or flow-limited perfusion.

However, the occlusions were kept short, i. Another potential limitation of our study is the lack of correlative regional myocardial perfusion quantification during the ischemic and reperfusion episodes. However, measurements made during a series of short-lived occlusions showed the typical response of acutely ischemic myocardium. All arguments thus suggest that the no-flow condition was met. At reperfusion, although not measured quantitatively, coronary re-flow was visually checked by aortic root angiography.

In this model of acute transmural infarction with TIMI 3 flow reperfusion, changes in wall thickness and thickening were complex. The primary function of the cardiac muscles is to stimulate contractions and relaxation in the heart. The contraction action results in the pumping of the blood from the ventricles to the whole body while the relaxation action of the cardiac muscles allows the atrium to receive blood.

This beating of the heart pumps the blood throughout the body ensuring that each cell and tissue of the body receives the blood supply. Cardiac muscles are essentially under the control of an autonomous nervous system that releases the timed nervous impulses signaling the heart cells to contract and relax in a rhythmic pattern. So, what actually happens in cardiac muscles when your heart beats?

Released Tropomyosin alters its position thereby allowing myosin to attach to actin. Myosin, then, utilizes the stored ATP molecules and reduce the length of each sarcomere.

The cardiac muscle undertakes twitch-type contractions wherein there is a long refractory period followed by brief relaxation periods. The relaxation action is vital for the heart in order to fill the atrium with blood for the next cycle. All the cardiac muscles work in harmony resulting in the generation of the force on the walls of the chamber of the heart.

The sheets of the cardiac muscles are placed in a planar fashion wherein each muscle is perpendicular to each other.

This creates the effect that when the heart contracts, it does so in multiple directions. Thus, contraction of the multiple layers of the cardiac muscle fiber results in the shrinkage of the ventricle and atrium from top to bottom as well as from side to side. This produces a strong pumping and twisting force in the ventricles, forcing blood throughout the body. It is important to note that cardiac muscle undergoes aerobic metabolism, principally utilizing lipids , and carbohydrates.

Myocardial dysfunction can be categorized into two types: primary due to genetic cause and secondary myocardial diseases mostly acquired causes but maybe precipitated due to genetic reasons.

Cardiomyopathies are diseases that result due to dysfunctional myocardium. Globally, cardiomyopathy is one of the foremost causes of morbidity and mortality. Clinically, cardiomyopathies can be categorized into five categories:. Very high quantity and continuous supply of oxygen and energy is the basic requirement of the cardiac tissues.

The oxygen supply is transported to the heart via the coronary arteries. However, these arteries are highly disposed to the formation of atheromas, i. Incase these atheromas are large, they obstruct or reduce the passage of the blood and oxygen to the cardiac cells thereby leading to the condition known as myocardial infarction or heart attack.

The reduction in the oxygen supply to the cardiac cells is known as myocardial ischemia. The lack of oxygen leads to the death of cardiac tissue. However, under the normal physiological response of the human body, the affected area gets repaired. Though the repairing leads to the formation of fibrous tissue at the site which disturbs the normal propagation and conduction of the excitatory stimuli resulting in abnormal contraction of the heart.

These asynchronous contractions result in cardiac arrhythmias i. Inflammation of the myocardium results in myocarditis. This can be attributed to a variety of causes viz. Injury and loss of both cardiomyocytes and cardiac vascular endothelial cells can occur in myocarditis. This results in the infiltration of the white blood cells into the heart muscle wall. This can eventually result in interstitial cardiac fibrosis, wall motion abnormalities, arrhythmias, heart failure, myocardial infarctions, reduced ejection fraction, and sudden cardiac death.

The human circulatory system is a double system, meaning there are two separate systems of blood flow: pulmonary circulation and systemic circulation. The adult human heart consists of two separated pumps, the right side right atrium and ventricle, which pumps deoxygenated blood into the pulmonary circulation, and the left side left atrium and ventricle , which pumps oxygenated blood into the systemic circulation.

Great vessels are the major vessels that carry blood into the heart and away from the heart to and from the pulmonary or systemic circuit. The great vessels collect and distribute blood across the body from numerous smaller vessels. The Systemic Circuit : The venae cavae and the aorta form the systemic circuit, which circulates blood to the head, extremities and abdomen.

The superior and inferior vena cava are collectively called the venae cavae. The venae cavae, along with the aorta, are the great vessels involved in systemic circulation. These veins return deoxygenated blood from the body into the heart, emptying it into the right atrium. The venae cavae are not separated from the right atrium by valves. The superior vena cava is a large, short vein that carries deoxygenated blood from the upper half of the body to the right atrium.

The right and left subclavian veins, jugular veins, and thyroid veins feed into the superior vena cava. The subclavian veins are significant because the thoracic lymphatic duct drains lymph fluid into the subclavian veins, making the superior vena cava a site of lymph fluid recirculation into the plasma.

The superior vena cava begins above the heart. The inferior vena cava is the largest vein in the body and carries deoxygenated blood from the lower half of the body into the heart. The left and right common iliac veins converge to form the inferior vena cava at its lowest point. The inferior vena cava begins posterior to the abdominal cavity and travels to the heart next to the abdominal aorta.

Along the way up the body from the iliac veins, the renal and suprarenal veins kidney and adrenal glands , lumbar veins from the back , and hepatic veins from the liver all drain into the inferior vena cava.

The aorta is the largest of the arteries in systemic circulation. Blood is pumped from the left ventricle through the aortic valve into the aorta. The aorta is a highly elastic artery and is able to dilate and constrict in response to blood pressure and volume.

When the left ventricle contracts to force blood through the aortic valve into the aorta, the aorta expands. This expansion provides potential energy to help maintain blood pressure during diastole, when the aorta passively contracts.

Blood pressure is highest in the aorta and diminishes through circulation, reaching its lowest points at the end of venous circulation. The difference in pressure between the aorta and right atrium accounts for blood flow in the circulation, as blood flows from areas of high pressure to areas of low pressure.

The aortic arch contains peripheral baroreceptors pressure sensors and chemoreceptors chemical sensors that relay information concerning blood pressure, blood pH, and carbon dioxide levels to the medulla oblongata of the brain. This information is processed by the brain and the autonomic nervous system mediates the homeostatic responses that involve feedback in the lungs and kidneys.

The aorta extends around the heart and travels downward, diverging into the iliac arteries. The five components of the aorta are:. The pulmonary arteries carry deoxygenated blood from the right ventricle into the alveolar capillaries of the lungs to unload carbon dioxide and take up oxygen. These are the only arteries that carry deoxygenated blood, and are considered arteries because they carry blood away from the heart.

The short, wide vessel branches into the left and right pulmonary arteries that deliver deoxygenated blood to the respective lungs. Blood first passes through the pulmonary valve as it is ejected into the pulmonary arteries.

Pulmonary circuit : Diagram of pulmonary circulation. Oxygen-rich blood is shown in red; oxygen-depleted blood in blue. The pulmonary veins carry oxygenated blood from the lungs to the left atrium of the heart. Despite carrying oxygenated blood, this great vessel is still considered a vein because it carries blood towards the heart. Four pulmonary veins enter the left atrium. The right pulmonary veins pass behind the right atrium and superior vena cava while the left pass in front of the descending thoracic aorta.

The pulmonary arteries and veins are both considered part of pulmonary circulation. The myocardium cardiac muscle is the thickest section of the heart wall and contains cardiomyocytes, the contractile cells of the heart. The myocardium, or cardiac muscle, is the thickest section of the heart wall and contains cardiomyocytes, the contractile cells of the heart.

As a type of muscle tissue, the myocardium is unique among all other muscle tissues in the human body. The structure of cardiac muscle shares some characteristics with skeletal muscle, but has many distinctive features of its own. Cardiomyocytes are shorter than skeletal myocytes and have fewer nuclei.

Each muscle fiber connects to the plasma membrane sarcolemma with distinctive tubules T-tubule. At these T-tubules, the sarcolemma is studded with a large number of calcium channels which allow calcium ion exchange at a rate much faster than that of the neuromuscular junction in skeletal muscle.

The flux of calcium ions into the muscle cells causes stimulates an action potential, which causes the cells to contract. Cardiac muscle, like skeletal muscle, is comprised of sarcomeres, the basic, contractile units of muscle. Sarcomeres are composed of long, fibrous proteins that slide past each other when the muscles contract and relax. Two of the important proteins found in sarcomeres are myosin, which forms the thick filament, and actin, which forms the thin filament.

Myosin has a long, fibrous tail and a globular head that binds to actin. The myosin head also binds to ATP, the source of energy for cellular metabolism, and is required for the cardiomyocytes to sustain themselves and function normally. Together, myosin and actin form myofibril filaments, the elongated, contractile threads found in muscle tissue. Cardiac muscle and skeletal muscle both contain the protein myoglobin, which stores oxygen.

Cardiac muscle is adapted to be highly resistant to fatigue. Cardiomyocytes have a large number of mitochondria, enabling continuous aerobic respiration. Cardiac muscle also has a large blood supply relative to its size, which provides a continuous stream of nutrients and oxygen while providing ample removal of metabolic waste. Cardiac Muscle : The tissue structure of cardiac muscle contains sarcomeres that are made of myofibrils with intercalated disks, that contain cardiomyocytes and have many mitocondria.

The myocardium has variable levels of thickness within the heart. Chambers of the heart with a thicker myocardium are able to pump blood with more pressure and force compared to chambers of the heart with a thinner myocardium. The myocardium is thinnest within the atria, as these chambers primarily fill through passive blood flow.

The right ventricle myocardium is thicker than the atrial myocardium, as this muscle must pump all blood returning to the heart into the lungs for oxygenation. The myocardium is thickest in the left ventricle, as this chamber must create substantial pressure to pump blood into the aorta and throughout systemic circulation. The thickness of the myocardium may change in some individuals as a compensatory adaptation to disease, either thickening and becoming stiff or becoming thinner and flabby.