inappropriate opening of the mitochondrial permeability transition pore (mptp) manifests in ischemia (blood flow restriction to tissue) and reperfusion injury (damage occurring after ischemia when blood flow returns to tissue), after myocardial infarction (heart attack) and when mutations in mitochondrial dna polymerase occur. the heart attempts to compensate for disease state by increasing the intracellular to increase the contractility cycling rates. constitutively high levels of mitochondrial cause inappropriate mptp opening leading to a decrease in the cardiac range of function, leading to cardiac hypertrophy as an attempt to compensate for the problem.