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The presence of diabetic cardiomyopathy and its relationship to concurrent hormonal and metabolic status have not been defined in patients with uncomplicated type I diabetes mellitus. Accordingly, radionuclide left ventricular angiograms and simultaneous metabolic profiles were obtained in 8 type I diabetic patients who had no major diabetic complications and in 11 normal subjects. Occult coronary artery disease was excluded by electrocardiogram exercise testing. Hemodynamics and systolic function did not differ between the groups. However, the peak filling rate (PFR; end-diastolic volumes per s) was less in the diabetic patients at rest [mean, 4.1 +/- 0.2 (+/- SE) vs. 4.8 +/- 0.2; P less than 0.05] and during aerobic (6.8 +/- 0.2 vs. 8.30 +/- 0.3; P less than 0.01) and anaerobic exercise (8.8 +/- 0.3 vs. 9.8 +/- 0.4; P less than 0.05). The time to PFR was prolonged in the diabetic patients at rest (174 +/- 10 vs. 133 +/- 7 ms; P less than 0.01) and during anaerobic exercise (126 +/- 5 vs. 103 +/- 6 ms; P less than 0.01). Plasma glucose and insulin levels were elevated in the diabetic patients at rest and during exercise. Otherwise, the metabolic and hormonal levels did not differ between the groups. In the diabetic patients, no single metabolic or hormonal parameter correlated with PFR or time to PFR. Impairment of diastolic filling also did not correlate with level of glycosylated hemoglobin or duration of diabetes. The alteration in diastolic filling present in type I diabetic patients who have no other diabetic complications may represent the earliest functional effect of diabetic cardiomyopathy.

Transient alterations in myocardial metabolism and ventricular function were observed after elective coronary bypass grafting despite apparently adequate intraoperative protection with cold potassium cardioplegia. Ninety patients had serial hemodynamic measurements and coronary sinus catheters inserted. Thirty-three patients had thermodilution coronary sinus flow catheters inserted to measure coronary sinus blood flow and to evaluate the myocardial utilization of oxygen and lactate. Nuclear ventriculograms were performed in 43 patients to assess ventricular function. Cardiac index fell after discontinuation of cardiopulmonary bypass and then rose between 2 and 24 hours postoperatively. Myocardial oxygen consumption steadily increased during this period. Myocardial lactate production reverted to lactate extraction 30 minutes after reperfusion. Reactive hyperemia was present during the first 10 minutes after cross-clamp release, and coronary sinus blood flow increased gradually during the first 24 hours postoperatively. The response to the stress of volume loading (the infusion of 250 to 500 ml of a colloid solution) and atrial pacing (at a rate of 110 beats/min) was evaluated 2 to 4 hours postoperatively (EARLY) and between 4 to 6 hours postoperatively (LATE). Volume loading resulted in a decrease in lactate extraction EARLY and an increase LATE (EARLY: -0.07 +/- 0.35 mmol/L; LATE: 0.08 +/- 0.32 mmol/L, mean +/- standard deviation not significant). Atrial pacing resulted in a decrease in lactate extraction EARLY and an increase LATE (EARLY: -0.11 +/- 0.34 mmol/L; LATE: 0.14 +/- 0.36 mmol/L, p less than 0.05). Diastolic compliance (the relation between the end-diastolic volume index) decreased between EARLY and LATE. Systolic function (the relation between the systolic blood pressure and the end-systolic volume index) and myocardial performance (the relation between the left ventricular stroke work index and the end-diastolic volume index) were unchanged. Ejection fraction correlated inversely with the end-diastolic volume index and did not represent an independent index of contractility. After elective coronary bypass grafting and cold crystalloid cardioplegia, myocardial metabolism recovered slowly. Hemodynamic stresses should be avoided in the early postoperative period to prevent progressive ischemic injury.

Hypertension following aorta-coronary bypass operations can contribute to myocardial ischemia. Nitroprusside therapy will reduce afterload, preload, and coronary perfusion pressure. Since both hypertension and its treatment can result in ischemic injury, nitroprusside must be carefully titrated to optimize cardiac function and metabolism. Thirty-one patients undergoing elective coronary bypass grafting were studied during a hypertensive episode (mean arterial pressure [MAP] = 119 +/- 18 mm Hg) and during nitroprusside therapy at an MAP of 97 +/- 11 mm Hg and at an MAP of 80 +/- 11 mm Hg (normotension). Nitroprusside also produced a significant (p less than 0.05) decrease in left atrial pressure (LAP), left ventricular end-diastolic volume index (EDVI) (stroke index divided by ejection fraction by nuclear angiography), stroke index, and stroke work index (SWI). Cardiac lactate extraction (LEx) and the ratio LEx/SWI increased (p less than 0.05) with the initial nitroprusside therapy, but lactate production resulted when the MAP was lowered to 80 mm Hg. Volume loading studies were performed during hypertension in four patients and during nitroprusside therapy in 15 patients. Neither performance nor compliance was significantly altered at an MAP of 97 mm Hg, but compliance decreased at normotension. Both hypertension and its treatment can result in inadequate myocardial metabolism. Nitroprusside should be titrated to maintain MAP between 90 and 100 mm Hg.