[Ventricular function in coronary heart disease].
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Biomedical subjects
Publications and source records attributed to P Rentrop.
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Actively contracting segments, preoperatively akinetic, were found in 8 of 63 patients, evaluated 6-12 months after aortocoronary surgery by coronary angiography. Ejection fraction was increased from 48.1% (S.D. 15.7) to 68.3% (S.D. 11.4). These patients are characterized by two simple clinical parameters: 1. All patients had angina pectoris at rest or at minimum exercise except for one; 2. preoperatively, there was a discrepancy between severe ventriculographic and discreet Ecg findings. These findings prove that myocardial function in coronary artery disease can be impaired at rest by ischemia, without clinical signs of coronary insufficiency, such as angina pectoris. Even severe impairment of left ventricular function is no contraindication for coronary artery surgery, if caused by reversible myocardial ischemia.
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Irreversible shock is produced in 28 anaesthetized mongrel dogs by withdrawal of erythrocytes and substitution by dextran, gelatine or plasma to an average Hb of 4.5g%. In contrast to other shock models cardiac output and perfusion pressure are not decreased by this preparation. In order to maintain arterial blood pressue above 90 mm Hg significantly more gelatine than dextran or serum has to be infused. There is no difference in hemodynamic responses after treatment with dextran or gelatine respectively. Both groups treated with colloidal solutions have the same survival rate of 38%. In the serum substituted dogs, however,survival rate is significantly greater (83%). Very likely this is due to a greater buffer capacity preventing severe acidosis, which is observed in the animals treated with colloidal solutions.
Ergometric and coronary angiographic findings were compared in 145 patients with proximal lesions of at least 50% of major coronary arteries. 75% of the patients had had a previous myocardial infarction. The following ergometric parameters occur most frequently in 3-vessel disease. (1) coronary insufficiency persisting after myocardial infarction, (2) ST-segment depression of at least 0.2 mV, (3) maximum exercise tolerance limited to less than 75 Watts. However, these parameters cannot predict 3-vessel disease with absolute certainty, nor can they exclude a single vessel disease. 3-vessel disease is not likely, if there is a maximum heart rate of 150 beats per minute or more. There were only slight differences between patients with 1-vessel disease and patients with 2-vessel disease. Patients who were limited at the 50 Watts level were found to have significant LAD disease, either alone or in combination with other vessels, with the exception of one patient.
Left ventricular filling pressure and cardiac output (C.O.) were studied at rest and during exercise in 145 patients with severe coronary artery disease, i.e. narrowing of at least one major coronary artery of greater than or equal to 50%. 95% of these patients had had a previous myocardial infarction. The most important findings are as follows: (1) Inappropriate C.O. at rest and during exercise indicates multiple vessel disease in most cases. (2) Marked increase of filling pressure during exercise indicates multiple vessel disease in most cases. (3) PCP during exercise is higher in patients with LAD disease (isolated or in combination with additional lesions), than in patients with RCA and/or left CX involvement.
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In patients with myocardial infarction (MI) the presence or absence of lesions in vessels other than the one which perfuses the infarcted area, has implications regarding coronary bypass surgery, long term anticoagulant therapy, work capacity and prognosis. We investigated whether involvement of a 2nd or 3rd vessels as demonstrated by coronary angiography can be predicted on the basis of angina pectoris and/or ischemic ST-segment depression during exercise. Inferior myocardial infarction (IMI, n = 146) Severe lesions (greater than or equal to 75%) of a 2nd or 3rd vessel were found in 61.7% of patients with IMI, who developed angina pectoris and ischemic ST-segment depression, in 18.6% of patients with ST-segment depression only, in 9.1% of patients with angina pectoris only and in 3.4% with neither angina pectoris nor ST-segment depression. Anteroseptal infarction (ASI, n = 116) Severe lesions (greater than or equal to 75%) of a 2nd or 3rd vessel were found in 30.2% of patients with ASI, who developed Angina pectoris and ischemic ST-segment depression; in 26.6% of patients with ST-segment depression only, in 20.0% of patients with angina pectoris only and in 3.0% of the patients with neither angina pectoris nor ST-segment depression. The clinical implications of the results are discussed.
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