LVH : Photo by: Srinivas Rao @ Gruppo dei Perfusionisti!!!
Ventricular Hypertrophy & Perfusion
Subendocardial Q Determinants
While subendocardial and sub-epicardial layers have the same determinants for blood flow, subendocardial layers are at greater risk from ischemia and infarction. The deeper subendocardium is subjected to greater wall tension which then expresses as a metabolic requirement 10-20% greater than the more superficial epicardium.
Higher oxygen demand and greater resistance to flow, diminishes the vasodilatory reserve in this layer making it vulnerable and pressure dependent when perfusion pressures fall below 70 mm Hg.
In conditions such as coronary stenosis where a pressure drop dictates pressure mediated flow to the subendocardium, blood flow to the epicardium may still be autoregulated (assuming a pressure in the outer layer of 40-60 mm Hg) and facilitate transmural coronary steal of blood flow to the epicardium
Healthy cardiac hypertrophy (physiologic hypertrophy or “athlete’s heart“) is the normal response to healthy exercise or pregnancy, which results in an increase in the heart’s muscle mass and pumping ability. Trained athletes have hearts that have left ventricular mass up to 60% greater than untrained subjects. Rowers, cyclists, and cross-country skiers tend to have the largest hearts, with an average left ventricular wall thickness of 1.3 centimeters, compared to 1.1 centimeters in average adults. Heart wall thickness can be measured by ultrasound; computed tomography is more accurate, though it is more expensive and has risks of exposure to radiation.
Unhealthy cardiac hypertrophy (pathological hypertrophy) is the response to stress or disease such as hypertension, heart muscle injury (myocardial infarction), heart failure or neurohormones. Valvular heart disease is another cause of pathological hypertrophy. It has also been suggested that the root cause of many heart ailments is cardiac hypertrophy, which in turn is caused by hypoxia due to atmospheric CO, particulate matter, and peroxyl acyl nitrates, which reduces ATP synthesis in cardiac mitochondria. Pathological hypertrophy also leads to an increase in muscle mass, but the muscle does not increase its pumping ability, and instead accumulates myocardial scarring (collagen). In pathological hypertrophy, the heart can increase its mass by up to 150%.
In most situations, described above, the increase in ventricular wall thickness is a slow process. However, in some instances hypertrophy may be “dramatic and rapid.”
In the Burmese python, consumption of a large meal is associated with an increase in metabolic work by a factor of seven and a 40% increase in ventricular mass within 48 hours, both of which return to normal within 28 days.
Aerobic training results in the heart’s being able to pump a larger volume of blood through an increase in the size of the ventricles. Anaerobic training results in the thickening of the myocardial wall to push blood through arteries compressed by muscular contraction. This type of physiologic hypertrophy is reversible and non-pathological, increasing the heart’s ability to circulate blood. Chronic hypertension causes pathological ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.