Biomedical subjects

E S Monrad

Publications and source records attributed to E S Monrad.

27 records · Page 2Linked to original sources

PubMed1987

Usefulness of percutaneous transluminal coronary angioplasty for unstable angina pectoris after non-Q-wave acute myocardial infarction.

Without revascularization, patients with non-Q-wave acute myocardial infarction (AMI) are predisposed to angina, recurrent AMI and cardiac death. Percutaneous transluminal coronary angioplasty (PTCA) was performed in 68 patients with angina an average of 2.3 months after non-Q-wave AMI (41 anterior, 27 inferior). Mean diameter stenosis was 95%, with collateralized total occlusion of the infarct-related artery in 23 patients. PTCA was successful in 87% (59 of 68), with a mean residual stenosis of 30%. One patient had emergency bypass surgery. Long-term follow-up (average 17 +/- 10 months) was available for 58 of the 59 patients in whom PTCA was successful. Recurrent angina developed in 41% (24 of 58), but was relieved by repeat PTCA in 14, by late coronary artery bypass surgery in 4 and by medical therapy in 6. There was 1 nonfatal AMI, due to progressive disease in a nondilated vessel, and 1 noncardiac death At last follow-up, 46 of 58 patients (79%) were asymptomatic and fully active or employed. Thus, patients undergoing PTCA for angina after non-Q-wave AMI appear to have a relatively high clinical restenosis rate, but with repeat PTCA have a low incidence of subsequent angina, AMI and cardiac death.

Adult↗

PubMed1987

The relationship of afterload to ejection performance in chronic mitral regurgitation.

Simultaneous left ventricular micromanometry and biplane cineangiography were performed in nine control subjects (group 1), 14 patients with chronic mitral regurgitation and an ejection fraction of 57% or greater (group 2), and 13 patients with mitral regurgitation and an ejection fraction of less than 57% (group 3). End-diastolic volume index was increased in both groups with mitral regurgitation (p less than .001) compared with the control group. Left ventricular end-diastolic wall thickness did not differ among the three groups, but the left ventricular muscle mass index was greater in both groups with mitral regurgitation than in controls (p less than .001). End-diastolic pressure was elevated in both groups 2 and 3 compared with group 1 (p less than .05), but peak systolic, mean systolic, and incisural pressure were not different among the three groups. End-diastolic stress was larger in groups 2 and 3 than in group 1 (p less than .05). Muscle fiber stretch was greater in group 2 than in the control group (p less than .05) but was not different between the controls and group 3. End-systolic stress, determined as the circumferential stress at aortic valve closure, at the maximal pressure/volume ratio, or using a nonsimultaneous method, was larger in group 3 than in groups 1 and 2. Mean systolic stress was evaluated from aortic valve opening to aortic valve closure in all patients; mean stress from end-diastole to aortic valve closure and from end-diastole to minimum volume was assessed in mitral regurgitation alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

Survival of patients with severe congestive heart failure treated with oral milrinone.

The safety and efficacy of long-term oral milrinone therapy were evaluated over a 2 1/2 year period in 100 patients who had severe congestive heart failure despite conventional therapy. Long-term oral milrinone therapy (27 +/- 8 mg/day initial dose) was well tolerated; drug-related side effects occurred in only 11% of patients and led to drug withdrawal in only 4% of patients. Of 94 patients evaluated after 1 month of therapy, 51% had improved by at least one New York Heart Association functional class. Despite hemodynamic and clinical improvements, life table analysis showed a 39% mortality rate at 6 months and a 63% mortality rate at 1 year of therapy. Characteristics at study entry that predicted death within 6 months included more advanced functional class, impaired renal function, lower right ventricular ejection fraction, presence of nonsustained ventricular tachycardia on 24 hour ambulatory electrocardiography, more impaired baseline hemodynamic function and absence of clinical improvement after 1 month of milrinone therapy. Multivariate analysis selected lower baseline cardiac index and aortic systolic pressure as the most significant variables in predicting death; patients who died of progressive heart failure had less frequent use of antiarrhythmic drugs and greater increases in furosemide and milrinone doses during long-term follow-up than did those who died suddenly. Thus, although milrinone is well tolerated and produces early symptomatic benefits in approximately half of patients with congestive heart failure refractory to conventional therapy, there is no evidence that it improves the high baseline mortality in this disorder.

Administration, Oral↗

PubMed1986

Therapy with cyclosporine in experimental murine myocarditis with encephalomyocarditis virus.

To explain the progression from infectious viral myocarditis to congestive cardiomyopathy an infection/immune hypothesis has been proposed stating that the primary viral process incites an excessive or disordered immunologic response against the myocardium. To test whether one form of immunosuppressive therapy might ameliorate this process, we used cyclosporine in a murine preparation of infectious myocarditis (encephalomyocarditis [EMC] virus), which has been shown to result in a congestive cardiomyopathy pathologically similar to that seen in man. Eight-week-old male DBA-2 mice were infected with EMC virus and randomized to a treatment or control group. Cyclosporine (25 mg/kg/day) was administered subcutaneously for 3 weeks, starting (1) at 1 week after infection during viral replication, and (2) at 3 weeks after infection, after the period of active viral replication. In mice treated during viral replication there was a significantly higher mortality rate compared with that of control mice (15/21 vs 9/29, p = .01). There was no evident reduction in myocardial pathology (inflammation, necrosis, or calcification) in the treated compared with the control groups. In mice treated after the period of viral replication, there was no improvement in mortality (8/22 vs 2/19, NS) compared with control. Treated mice showed no reduction in myocardial histopathologic lesions. Furthermore, treated mice had significantly greater heart weight/body weight ratios (1.3 +/- 0.4% vs 1.0 +/- 0.3%, p less than .005), lung weight/body weight ratios (1.1 +/- 0.5% vs 0.8 +/- 0.3%, p less than .05), and liver weight/body weight ratios (6.0 +/- 0.8% vs 5.4 +/- 0.6%, p less than .005) than control mice, suggesting more severe myocardial failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Milrinone, dobutamine, and nitroprusside: comparative effects on hemodynamics and myocardial energetics in patients with severe congestive heart failure.

To assess their comparative effects on hemodynamics and myocardial energetics, we administered nitroprusside (1.5 +/- 0.6 microgram/kg-min), dobutamine (10 +/- 3 micrograms/kg-min), and milrinone (67 +/- 13 micrograms/kg-min) sequentially to 10 patients with severe (NYHA class III or IV) congestive heart failure. Each agent led to a significant (p = .001) increase in cardiac index (1.9 +/- 0.5 to 2.7 +/- 0.6 liters/min/m2; 1.7 +/- 0.4 to 2.6 +/- 0.6 liters/min/m2; and 1.8 +/- 0.5 to 2.7 +/- 0.5 liters/min/m2, for nitroprusside, dobutamine, and milrinone, respectively). Dobutamine did not produce a significant change in the pulmonary capillary wedge pressure (27 +/- 5 to 24 +/- 6 mm Hg, NS) nor in mean arterial pressure (83 +/- 9 to 86 +/- 10 mm Hg, NS), but caused a significant rise in heart rate (85 +/- 16 to 99 +/- 17 beats/min, p = .001) and in myocardial oxygen consumption (8.7 +/- 2.1 to 11.1 +/- 3.8 ml O2/min, p = .03). In contrast, nitroprusside and milrinone each caused a significant (p = .001) fall in the pulmonary capillary wedge pressure (27 +/- 6 to 19 +/- 7 mm Hg and 26 +/- 6 to 19 +/- 9 mm Hg, respectively), without significantly increasing either the heart rate (87 +/- 18 to 85 +/- 17 beats/min and 86 +/- 17 to 89 +/- 17 beats/min, respectively) or myocardial oxygen consumption (8.8 +/- 2.3 to 7.6 +/- 2.1 ml O2/min and 8.8 +/- 2.1 to 8.4 +/- 2.1 ml O2/min, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗

PubMed1986

Assessment of long-term therapy with milrinone and the effects of milrinone withdrawal.

To assess the long-term efficacy of milrinone in patients with severe congestive heart failure, we obtained hemodynamic measurements (systemic arterial and right heart catheterization) in 13 patients at baseline and after intravenous administration of milrinone. After continuous oral milrinone therapy of 8 +/- 4 months duration, repeat hemodynamic study was performed in patients on oral milrinone therapy, after withdrawal of milrinone, and after readministration of milrinone intravenously. Comparison of initial baseline and withdrawal hemodynamic measurements for the group as a whole showed no interval progression of heart failure, as reflected by the pulmonary capillary wedge pressure (27 +/- 8 to 24 +/- 12 mm Hg, NS) or the cardiac index (2.0 +/- 0.4 to 2.1 +/- 0.8 liters/min/m2, NS). Individual comparisons of milrinone-free hemodynamics revealed that five patients had improved hemodynamically, three patients were unchanged, and five patients had deteriorated, four of whom manifested dependence on milrinone with a progressive hemodynamic decline after milrinone withdrawal which required readministration of milrinone on an emergency basis. Continued efficacy of milrinone was observed on readmission after withdrawal: pulmonary capillary wedge pressure fell from 27 +/- 8 to 16 +/- 10 mm Hg (p = .001) initially and from 24 +/- 12 to 13 +/- 11 mm Hg (p = .001) at readministration, while cardiac index rose from 2.0 +/- 0.4 to 2.8 +/- 0.5 liters/min/m2 (p = .001) initially and from 2.1 +/- 0.8 to 2.7 +/- 0.5 liters/min/m2 (p = .005) upon readministration.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1985

Effects of milrinone on coronary hemodynamics and myocardial energetics in patients with congestive heart failure.

To examine the effect of milrinone on myocardial energetics in patients with congestive heart failure, we measured systemic, pulmonary, and coronary hemodynamics in 18 patients before and after intravenous administration of milrinone (125 +/- 36 micrograms/kg). There was a 45% increase in cardiac index (2.1 +/- 0.5 to 3.0 +/- 0.6 liters/min/m2; p = .0001), a 39% fall in the pulmonary capillary wedge pressure (28 +/- 8 to 17 +/- 8 mm Hg; p = .0001), and a 42% increase in left ventricular external work (3758 +/- 1419 to 5340 +/- 1598 g-m/min; p = .0001). Both the heart rate-blood pressure product (9624 +/- 2272 to 9380 +/- 2428 mm Hg-beats/min; p = NS) and regional left ventricular myocardial oxygen consumption (7.6 +/- 2.9 to 8.1 +/- 3.1 ml O2/min; p = NS) were unchanged after milrinone, resulting in a 45% increase in calculated left ventricular external efficiency (p = .004). Although myocardial oxygen consumption did not change, regional great cardiac venous blood flow increased significantly (73 +/- 32 to 85 +/- 34 ml/min; p = .02) as a result of a 30% reduction in regional coronary vascular resistance (1.32 +/- 0.99 to 0.93 +/- 0.54 mm Hg-min/ml; p = .004), a decrease comparable to the concurrent 37% and 38% falls seen in systemic and pulmonary vascular resistance, respectively. These changes were associated with an 11% fall in the transcoronary arterial-venous oxygen difference (111 +/- 24 to 99 +/- 21 ml/O2/liter; p = .0001), which is consistent with a primary coronary vasodilator effect of milrinone.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

PubMed1984

Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.

To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased (+ 18%; p less than .01) and T decreased (-30%; p less than .01), while heart rate increased by only 8% (87 +/- 12 to 94 +/- 15 beats/min; p less than .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p less than .01). Left ventricular peak filling rate increased (1.2 +/- 0.6 to 1.7 +/- 0.7 end-diastolic volumes/sec; p less than or equal to .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 +/- 7 to 18 +/- 9 mm Hg; p less than .01). There was a fall in left ventricular end-diastolic pressure (28.6 +/- 6 to 19 +/- 7 mm Hg; p less than or equal to .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1983

Evaluation of a new bipyridine inotropic agent--milrinone--in patients with severe congestive heart failure.

Milrinone, a derivative of amrinone, has nearly 20 times the inotropic potency of the parent compound and does not cause fever or thrombocytopenia in normal volunteers or in animals sensitive to amrinone. In 20 patients with severe congestive heart failure, intravenous milrinone resulted in significant decreases in left ventricular end-diastolic pressure (from 27 +/- 2 to 18 +/- 2 mm Hg), pulmonary wedge pressure, right atrial pressure, and systemic vascular resistance, as well as a slight reduction in mean arterial pressure. Significant increases occurred in cardiac index (from 1.9 +/- 0.1 to 2.9 +/- 0.2 liters per minute per square meter) and the peak positive first derivative of left ventricular pressure, with a slight increase in heart rate. Hemodynamic improvement was sustained during a 24-hour continuous infusion. Nineteen of the 20 patients subsequently received oral milrinone (29 +/- 2 mg per day) for up to 11 months (mean, 6.0 +/- 0.8), with sustained improvement in symptoms of heart failure. In 10 patients receiving long-term oral milrinone (greater than or equal to 6 months) radionuclide ventriculography showed continued responsiveness, with a 27 per cent increase in left ventricular ejection fraction after 7.5 mg of the drug. Four patients died after a mean of 4.8 months of therapy, and three patients with severe underlying coronary-artery disease and angina pectoris required additional antianginal therapy. No patient had fever, thrombocytopenia, gastrointestinal intolerance, or aggravation of ventricular ectopy. We conclude that milrinone shows promise for the longterm treatment of congestive heart failure.

Administration, Oral↗