What is the pathophysiology of dilated cardiomyopathy?

Updated: Mar 02, 2021
  • Author: Vinh Q Nguyen, MD, FACC; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...
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Dilated cardiomyopathy is characterized by ventricular chamber enlargement and systolic dysfunction with greater left ventricular (LV) cavity size with little or no wall hypertrophy. Hypertrophy can be judged as the ratio of LV mass to cavity size; this ratio is decreased in persons with dilated cardiomyopathies.

The enlargement of the remaining heart chambers is primarily due to LV failure, but it may be secondary to the primary cardiomyopathic process. Dilated cardiomyopathies are associated with both systolic and diastolic dysfunction. The decrease in systolic function is by far the primary abnormality due to adverse myocardial remodeling that eventually leads to an increase in the end-diastolic and end-systolic volumes.

Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further diminish the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction.

Early compensation for systolic dysfunction and decreased cardiac output is accomplished by increasing the stroke volume, the heart rate, or both (cardiac output = stroke volume × heart rate), which is also accompanied by an increase in peripheral vascular tone. The increase in peripheral tone helps maintain appropriate blood pressure. Also observed is an increased tissue oxygen extraction rate with a shift in the hemoglobin dissociation curve.

In decompensation of systolic heart failure, several changes in the pressure-volume (P-V) curve are seen. The entire P-V loop shifts to the right with an increased in end-diastolic pressure and end-diastolic volume. Coronary blood flow may also be impaired by hypotension and elevated wall stress, decreasing the perfusion gradient.

The basis for compensation of low cardiac output is explained by the Frank-Starling Law, which states that myocardial force at end-diastole compared with end-systole increases as muscle length increases, thereby generating a greater amount of force as the muscle is stretched. Overstretching, however, leads to failure of the myocardial contractile unit.

These compensatory mechanisms are blunted in persons with dilated cardiomyopathies, as compared with persons with normal LV systolic function. Additionally, these compensatory mechanisms lead to further myocardial injury, dysfunction, and geometric remodeling (concentric or eccentric).

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