When the heart contracts against an increased pressure, as occurs with hypertension or an obstructed outflow tract (e.g., stenosis of the aortic valve), the growth appears to occur inward, tending to obliterate the ventricular lumen. This process normalizes the stress on the individual fibers by thickening the ventricular wall. Such a pattern of hypertrophy is termed concentric hypertrophy (Fig. 3). Stretch receptors in the muscle cells detect when the fibers are under an elevated load and stimulate signal transduction pathways involving protein kinases to increase the production of new contractile proteins within minutes of the onset of the stretch. Angiotensin II has also been implicated in contributing to the remodeling process, as its receptors stimulate the protein kinases as well. Drugs that block the action of angiotensin II are particularly effective in patients with hypertension because they not only reduce the blood pressure but also directly interfere with the hypertrophy process within the heart. The thickened ventricular wall of the concentrically hypertrophied heart decreases diastolic compliance
FIGURE 3 Transverse section of three ventricles, one normal and two hypertrophied. Chronic pressure overload causes a remodeling of the heart, called concentric hypertrophy, in which the heart has a thick wall and small lumen. Chronic volume overload leads to eccentric hypertrophy, in which the diameter of the lumen is increased along with the muscle mass.
and the small lumen limits the stroke volume; thus, a total compensation cannot be achieved by hypertrophy. If the underlying cause is not corrected, such a heart will eventually experience a positive feedback spiral to failure, leading to the eventual death of the patient.
When the heart ejects against a normal pressure but has an elevated stroke volume, it responds by keeping the wall thickness relatively constant but increasing the diameter of the lumen. Such a pattern is termed eccentric hypertrophy (see Fig. 3). Generally, this pattern of hypertrophy is better tolerated because the diastolic compliance is not lost. In fact, a mild eccentric hypertrophy is often seen in athletes and causes no serious problem. When moderate to severe eccentric hypertrophy occurs in response to a regurgitant aortic or mitral valve, however, the heart will progress to failure. When failure does occur in such a heart, it is difficult to treat. Unlike the case with the heart that hypertrophies in response to a high pressure, correcting the regurgitant valve usually increases rather than decreases the pressure against which the heart must eject, which will exacerbate the failure condition. As a result, the condition must be corrected before the heart becomes too weakened.
Heart failure can occur in the absence of an elevated workload, as occurs in myopathic conditions. In these cases, there is a progressive weakening of the heart; in severe cases, the only effective treatment may be a heart transplant. Genetic defects that cause the heart to make one or more defective proteins are now known to underlie some of the cardiomyopathies.
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