Dean J. Kereiakes

Myocarditis and cardiomyopathy

With more widespread application of EMB techniques, a significant percentage of ICCM patients have been found to have lymphocytic myocarditis on biopsy. It is now appreciated that patients with myocarditis may also present with isolated abnormalities of left ventricular diastolic function, dysrhythmias, and/or complaints of chest discomfort with normal coronary angiograms. Epidemiologic and serologic data incriminate a viral etiology underlying many cases of acute myocarditis and ICCM. Although most cases of viral myocarditis appear to resolve without residual left ventricular dysfunction, a small but significant percentage of these patients progress to chronic congestive cardiomyopathy. In the absence of persistent active viral infection in these patients, myocardial damage may be mediated by both cellular and humoral immune mechanisms. The concept of virus-induced immune mediated myocardial damage forms the basis for attempts at immunosuppressive therapy. Whether immunosuppressive therapy alters the natural history of myocarditis is at present unknown and awaits demonstration by a controlled clinical trial.

Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure

To evaluate changes in myocardial energetics and systemic and cardiac sympathetic activity associated with improved left ventricular function after MDL 17043, a new inotropic vasodilator agent, systemic and coronary hemodynamics and myocardial catecholamine balance were determined in 17 patients with severe heart failure. After the administration of MDL 17043, cardiac index increased by 67% and pulmonary capillary wedge pressure decreased (25 +/- 5 to 14 +/- 7 mm Hg, p less than 0.01), indicating improved left ventricular function. Coronary sinus blood flow (75 +/- 29 to 111 +/- 51 ml/min, p less than 0.01) and myocardial oxygen consumption (9.9 +/- 3.3 to 11.8 +/- 5.4 ml/min, p less than 0.05) increased despite decreased myocardial oxygen extraction (11.7 +/- 2 to 10.1 +/- 3.3 vol%, p less than 0.05) and a higher coronary sinus oxygen content. Although transmyocardial lactate extraction remained unchanged, increased myocardial oxygen consumption has potential deleterious effects on myocardial metabolic function. Arterial norepinephrine concentrations and transmyocardial norepinephrine release also remained unchanged. These findings suggest that MDL 17043 improves left ventricular pump function, but produces no detectable change in systemic and cardiac sympathetic activity. Improved left ventricular function is associated with increased myocardial oxygen consumption despite primary coronary vasodilation.

Mechanisms of improved left ventricular function following intravenous MDL 17,043 in patients with severe chronic heart failure

To evaluate the mechanisms for improved left ventricular function with MDL 17,043 in patients with severe chronic heart failure, 24 patients were evaluated by simultaneous determination of hemodynamics by right heart catheterization and ejection fraction by computerized nuclear probe before and following intravenous administration of MDL 17,043 (mean cumulative dose 3.6 mg/kg). Following MDL 17,043, there was an increase in cardiac index (+62%), stroke volume index (+42%), and stroke work index (+68%), together with a decrease in pulmonary capillary wedge pressure (-46%), indicating improved left ventricular pump function. There was a marked reduction in systemic vascular resistance (-40%) and a modest reduction in arterial pressure, indicating decreased left ventricular outflow resistance. The ratio of peak systolic blood pressure to calculated left ventricular end-systolic volume tended to increase, but the change was not statistically significant. Despite a marked increment in stroke volume index, left ventricular ejection time corrected for heart rate was shortened, suggesting enhanced contractility. In the group as a whole, the calculated left ventricular end-diastolic volume remained unchanged, but it increased in 14 patients. Since pulmonary capillary wedge pressure fell in each patient, this suggests improved overall left ventricular distensibility. Thus, decreased left ventricular outflow resistance, and possibly increased contractile function, and improved left ventricular diastolic compliance may all contribute to improved left ventricular pump function with MDL 17,043 in patients with severe heart failure.

Percutaneous transluminal angioplasty of left internal mammary artery grafts

Abstract Recent data have demonstrated the superior long-term patency of left internal mammary artery (IMA) grafts compared with saphenous vein (SV) grafts, making the left IMA a preferable choice, particularly in younger patients. 1–3 Percutaneous transluminal angioplasty (PTA) can successfully dilate SV graft stenoses after bypass surgery. 4 This report describes the successful PTA of left IMA grafts in 2 patients.

Potential mechanisms of improved left ventricular function with enoximone in severe congestive heart failure

Enoximone, a phosphodiesterase inhibitor, is a potent inotropic vasodilator agent that causes a marked improvement in systemic hemodynamics in patients with severe chronic congestive heart failure. Cardiac index, stroke volume index and stroke work index increase, and there is a significant decrease in pulmonary capillary wedge pressure. Left ventricular dP/dt increases, despite a decrease in arterial pressure and systemic vascular resistance and without any significant change in heart rate, indicating a positive inotropic effect. A marked decrease in systemic vascular resistance indicates that decreased left ventricular outflow resistance resulting from peripheral vasodilation also contributes to improvement in left ventricular function. In some patients, left ventricular end-diastolic volume increases despite a marked decrease in pulmonary capillary wedge pressure, suggesting an improvement in apparent left ventricular compliance, which may also be contributory to improved left ventricular function.

Right ventricular myocardial infarction with ventricular septal rupture

Since the original description of Cohn et al.,’ the syndrome of right ventricular myocardial infarction (RVMI) complicating inferior myocardial infarction has been the focus of extensive investigation. Various noninvasive techniques have been applied to aid in early diagnosis,2 and a characteristic hemodynamic profile of central venous pressure elevation with a noncompliant pattern in the right atria1 pressure record and close proximity of right atrial and pulmonary capillary wedge pressures has been described.3 Although RVMI has been reported in association with myocardial rupture’ and right-to-left shunting through a patent foramen ovalet associated ventricular septal rupture (VSR) has received relatively little attention.6 We report the hemodynamic profile and clinical course of four patients with VSR complicating RVMI seen at our institution over the past 4 years. The clinical characteristics of these four patients are shown in Table I. All patients demonstrated acute inferior myocardial infarction on the ECG and in one case, new right bundle branch block was noted. All patients had balloon-tipped, flow-directed pulmonary arterial catheters inserted, and measurements of right atrial and pulmonary capillary wedge pressures, thermodilution cardiac outputs, and pulmonary-systemic shunt ratios (Qp/Qs) by oximetry immediately following the diagnosis of septal rupture are listed in Table II. In each case, evidence of severe right ventricular (RV) dysfunction was demonstrated. The clinical and hemodynamic findings of RVMI were confirmed by noninvasive evaluation in each patient as illustrated in Fig. 1. The time from symptomatic onset of myocardial infarction to the development of VSR ranged from 1 to 4 days. Septal rupture was heralded by the occurrence of new pansystolic murmur at the left sternal border and was associated with palpable thrill in two cases. Two patients underwent preoperative coronary angiography. In both patients, the right coronary artery was occluded proximally. Patient No. 2 had associated significant stenoses of the left anterior descending and circumflex coronary arteries, and patient No. 4 had an associated stenosis of the circumflex coronary artery.