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Biomedical subjects

A Marmor

Publications and source records attributed to A Marmor.

At least 37 records · Page 2Linked to original sources
PubMed1993

Left ventricular peak power during exercise: a noninvasive approach for assessment of contractile reserve.

Cardiac peak power, a contractility index based upon instantaneous changes in intracavitary pressure and systolic peak flow, was measured at rest and during supine exercise in 26 patients with coronary artery disease and 8 healthy subjects. The pathophysiological significance of this index was compared with left ventricular ejection fraction (LVEF) during exercise. Cardiac peak power, ejection fraction, end-diastolic volume, stroke volume, cardiac output and systemic vascular resistance were measured at rest, during three stages of supine bicycle ergometry and two stages of recovery. Cardiac peak power increased continuously in healthy subjects, from 5.4 +/- 0.8 W/ml at rest to 11.4 +/- 3.1 W/ml at peak exercise, p < 0.001. In patients, peak power increased initially, reached a plateau in stage 2, and subsequently remained unchanged in stage 3 (5.6 +/- 2 versus 5.6 +/- 1.6 W/ml, p = ns). Ejection fraction demonstrated a flat response during exercise in patients, contrasting with a 42% increase in cardiac peak power. The lack of increase in ejection fraction was attributed to its dependence on afterload. Peak power showed no correlation with systemic vascular resistance (r = 0.01, p = ns). In a subgroup of patients with low resting LVEF (LVEF = 26% +/- 7%), peak power increased 70% during exercise, from 2.0 +/- 0.7 to 3.5 +/- 1.7 W/ml, p < 0.05, in contrast to a flat ejection fraction response. Thus, cardiac peak power, a relatively afterload-independent index of left ventricular performance and contractility can be obtained noninvasively during exercise.

Blood Pressure↗
PubMed1991

Electrocardiogram changes during intrauterine injection of ionic contrast medium.

The effect of intrauterine injection of meglumine-sodium diatrizoate 60% on the electrocardiogram was studied in 28 young, healthy women during routine hysterosalpingography. The most important single finding observed was significant QTc prolongation in 25 (90%) out of the 28 women examined. QTc increased from 417 +/- 18 mseconds to 451 +/- 30 mseconds (P less than .001). This effect disappeared rapidly within 2 to 3 minutes. Saline was injected in ten women prior to contrast medium injection in order to exclude direct mechanical dilatatory effect of the injected material. The QTc did not change significantly after saline (418 +/- 18 mseconds). The mechanism involved in the QTc prolongation is not known.

Adult↗
PubMed1990

Prevention of creatine kinase-MB release in coronary artery disease and pacing-induced myocardial ischemia by isosorbide dinitrate spray.

The effect of isosorbide dinitrate (ISDN) spray on release of the isoenzyme creatine kinase-MB (CK-MB) after myocardial ischemia induced by atrial pacing was evaluated in 8 patients with coronary artery disease. Atrial pacing to ischemia (ST-segment depression of greater than or equal to 1.5 mm for greater than or equal to 80 ms) resulted in elevation of CK-MB levels in plasma drawn from the coronary sinus, from 1.8 +/- 1.5 to 6.8 +/- 7.0 ng/ml (p less than 0.001) at 30 minutes after onset of ischemia. When atrial pacing was repeated at the same rate after 1 squirt of ISDN spray, 1.25 mg, the CK-MB levels were not altered despite significant ischemic ST-segment depression. It is concluded that ISDN prevents the process responsible for myocardial release of CK-MB, being either micronecroses or a reversible consequence of ischemia.

Administration, Oral↗
PubMed1990

Comparative evaluation of a new formulation of isosorbide dinitrate oral spray and sublingual nitroglycerin tablets.

The magnitude and time course of the hemodynamic effect of a new formulation of an aqueous solution of isosorbide dinitrate (ISDN) spray were compared with those of sublingual nitroglycerin (NTG) tablets in 12 patients with chronic congestive heart failure. The patients received, in a random order, ISDN spray, 2.5 mg, or sublingual NTG, 0.8 mg. Hemodynamic measurements were performed before and at 1, 3, 5, 10, 20, 30 and 60 minutes after each drug. The second drug was given only after return of the hemodynamic parameters to baseline, plus a washout period of 2 hours. The hemodynamic variables measured were comparable at baseline. Both drugs produced hemodynamic improvement including a decrease in pulmonary capillary wedge pressure (PCWP), right atrial pressure and systemic and pulmonary vascular resistances. Only ISDN spray significantly increased cardiac output. The onset of action of ISDN spray was significantly more rapid than that of NTG. This was primarily evident in the decrease in PCWP. With ISDN spray the decrease started at 1 minute after administration, and at 3 minutes a decrease of 8.6 mm Hg was already found. The corresponding value for sublingual NTG was 1.6 mm Hg. The difference was highly significant (p less than 0.02). The peak effect of ISDN spray on PCWP and right atrial pressure was greater than that of NTG. Thus, the onset of the hemodynamic effect of the new formulation of ISDN spray is much more rapid than that of sublingual NTG tablets. At the doses used, the magnitude of the effect of the ISDN spray on some of the hemodynamic variables is greater than that of sublingual NTG.

Administration, Oral↗
PubMed1990

Comparison of the acute effects of captopril and of nifedipine on left ventricular diastolic function in elderly hypertensive patients.

The acute effects of single doses of captopril (C) 12.5 mg, of nifedipine (N) 10 mg, or of their combination (C + N) on parameters of left ventricular (LV) function were assessed in 18 elderly hypertensive subjects using radionuclide ventriculography. Blood pressure (BP) was lowered by C from 177/100 to 164/92 mmHg, by N from 177/100 to 161/91 mmHg (p less than 0.02/less than 0.05 for both C and N) and by C + N from 176/100 to 151/83 mmHg (p less than 0.01/less than 0.01). Nifedipine accelerated heart rate from 74 to 85 and C + N from 74 to 82 beats/min (p less than 0.01 in both cases), whereas C left it unchanged. Left ventricular ejection fraction (EF) was not significantly affected by either drug alone or by both drugs combined. Peak ejection rate (PER) and peak filling rate (PFR) were slightly, but not significantly, enhanced by all treatments. Captopril shortened the time to peak filling rate (TPFR) by 21 msec (p less than 0.05), N by 26 msec (p less than 0.01) and their combination by 22 msec (p less than 0.05); however, when corrected for RR interval or length of diastole, TPFR was shortened only by C (p less than 0.05). Tachycardia induced by acute administration of N may have an unwanted effect on LV diastolic function, which can be partially blunted by the concomitant administration of a converting enzyme inhibitor.

Aged↗
PubMed1990

Comparative evaluation of the acute and chronic effects of cilazapril and hydrochlorothiazide on diastolic cardiac function in hypertensive patients.

UNLABELLED: The effect of cilazapril, 2.5 to 5.0 mg and hydrochlorothiazide, 25 to 50 mg, on diastolic cardiac function was studied by echocardiography and radionuclide ventriculography, using a double-blind randomized parallel-group design with a placebo run-in period, in 30 hypertensive patients. The measurements were made before and three hours after the first dose, and after ten weeks of treatment. Both drugs lowered the elevated blood pressure and did not impair the normal systolic cardiac function. In the patients treated with cilazapril an improvement in indices of diastolic function was observed after the first dose. The normalized peak filling rate significantly increased from 2.4 +/- 0.7 to 2.7 +/- 0.7 counts and time to peak filling rate was shortened from 169.4 +/- 31.0 to 151.6 +/- 40.1 msec. This improvement was sustained or even enhanced during chronic therapy. In contrast hydrochlorothiazide acutely impaired one index of diastolic function, the normalised peak filling rate, and did not alter the other indices. Long-term treatment with cilazapril, but not with hydrochlorothiazide, caused regression of left ventricular hypertrophy. IN CONCLUSION: cilazapril is superior to hydrochlorothiazide in its effect on diastolic cardiac function in hypertensive patients. The beneficial effect is partially related to regression of left ventricular hypertrophy.

Aged↗
PubMed1990

The acute and chronic effects of cilazapril on cardiac function in hypertensive patients.

UNLABELLED: The effect of cilazapril, 2.5 to 5.0 mg on systolic and diastolic cardiac function was studied by echocardiography and radionuclide ventriculography, in 15 hypertensive patients. The measurements were made before and 3 hours after the first dose, and after 10 weeks of treatment. Cilazapril lowered the elevated blood pressure and did not affect the normal ejection fraction. An improvement in indices of diastolic function was observed after the first dose. The normalized peak filling rate significantly increased from 2.4 +/- 0.7 to 2.7 +/- 0.7 counts and time to peak filling rate was shortened from 169.4 +/- 31.0 to 151.6 +/- 40.1 msec. This improvement was sustained or even enhanced during chronic therapy. Long-term treatment with cilazapril, caused regression of left ventricular hypertrophy. IN CONCLUSION: cilazapril improves diastolic cardiac function in hypertensive patients. The beneficial effect may be partially related to regression of left ventricular hypertrophy.

Aged↗
PubMed1989

A single dose of cilazapril improves diastolic function in hypertensive patients.

We studied the effect of a single dose of cilazapril, 5.0 mg orally, on systolic and diastolic cardiac function in eight hypertensive patients using a double-blind crossover placebo-controlled design. All patients had concentric left ventricular hypertrophy (measured by echocardiography), unimpaired systolic function (measured by radionuclide ventriculography), and long-standing hypertension treated by a combination of beta-blockers and diuretics. Radionuclide scintigraphy was performed with cilazapril and placebo, given one week apart. A two-week washout period of all cardioactive drugs preceded the study. Within three hours after oral administration of cilazapril, the time to peak filling rate of the left ventricle, expressed as a percentage of diastole, was reduced from 44.5 +/- 13.2 percent to 31.2 +/- 7.2 percent (p less than 0.05). Systolic blood pressure was also significantly reduced by cilazapril. Heart rate was slightly reduced. Left ventricular ejection fraction, peak filling rate, and the absolute time to peak filling rate were not significantly altered. Cilazapril improves a sensitive index of diastolic cardiac function in hypertensive patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Effects of a single dose of isosorbide-5-mononitrate on the left ventricular diastolic function in systemic hypertension.

The effect of a single dose of isosorbide-5-mononitrate on left ventricular (LV) diastolic function was assessed by radionuclide ventriculography in 18 hypertensive patients. The effect of the mononitrate on atrial filling also was assessed. As expected, there was a significant decrease in mean blood pressure (120 +/- 17 to 102 +/- 18 mm Hg, p less than 0.005). Global LV ejection fraction did not show a significant change, increasing slightly from 64 +/- 9 to 68 +/- 8% (difference not significant). The mononitrate prolonged the time to peak filling rate from 176 +/- 36 to 195 +/- 29 ms (p less than 0.0001). The percentage of time to peak filling rate from diastole also increased, from 46 to 53% (p less than 0.05), whereas the normalized peak filling rate did not change (2.36 +/- 0.6 to 2.31 +/- 0.6 end-diastolic volumes/s, difference not significant). This effect on LV diastolic function was closely related to a certain reduction in preload, as suggested by the reduction in mean left atrial filling (45 +/- 12 to 40 +/- 13 counts/s, p less than 0.005) and LV diastolic counts, suggesting that the "impairment" of diastolic function induced by nitrates is secondary to the reduction in venous return to the left atrium. The mononitrate did not affect the mean right atrial filling rate (50 +/- 12 to 52 +/- 13 counts/s) and the right ventricular end-diastolic counts, suggesting a primary vasodilatory effect of nitrates on the pulmonary vascular bed.

Adult↗
PubMed1989

The effect of flosequinan in patients with heart failure of acute onset complicating acute myocardial infarction.

We studied the hemodynamic effect of a single dose of the new direct-acting vasodilator, flosequinan, in 18 patients with severe heart failure of acute onset complicating acute myocardial infarction, which was resistant to high doses of diuretics, nitrates and dobutamine given intravenously. Flosequinan was added to conventional therapy at 3.5 +/- 0.8 days from the infarction, in the form of a single oral dose of 100 mg. Hemodynamic measurements were performed every hour for 4 hours after the administration, without any other drug being added. The infusion rate of nitrates was kept constant. Flosequinan produced hemodynamic improvement in this group. The effect peaked at 2 hours and remained at this level at 4 hours. Pulmonary capillary wedge pressure decreased from 27.6 +/- 4.3 to 16.8 +/- 2.8 mm Hg and cardiac output increased from 3.5 +/- 0.3 to 4.1 +/- 0.4 l/min (P less than 0.001). Pulmonary arterial and right atrial pressures and systemic and pulmonary vascular resistances were also significantly reduced. Heart rate and mean systemic arterial pressure were not significantly altered. Administration of flosequinan was not associated with symptomatic hypotension, cardiac arrhythmias or other adverse events. We conclude that flosequinan is effective in producing acute hemodynamic improvement in patients with heart failure, complicating acute myocardial infarction, which is resistant to conventional therapy. Flosequinan is safe and well tolerated. Studies for longer time periods are indicated.

Acute Disease↗
PubMed1989

Effect of flosequinan in patients with acute-onset heart failure complicating acute myocardial infarction.

We studied the hemodynamic effect of a single dose of the new direct-acting vasodilator, flosequinan, in ten patients with severe acute-onset heart failure complicating acute myocardial infarction (MI) resistant to high iv doses of diuretics, nitrates, and dobutamine. Flosequinan was added to conventional therapy at 3.8 +/- 0.5 days after infarction in the form of a single 100-mg oral dose. Hemodynamic measurements were performed every hour for 4 h after administration, without any other drug being added. The nitrate infusion rate was kept constant. Flosequinan produced hemodynamic improvement in this group. The effect peaked at 1 to 2 h and remained at this level at 4 h. Pulmonary capillary wedge pressure decreased from 27.2 +/- 5.4 to 16.4 +/- 3.0 mm Hg, and cardiac output increased from 3.5 +/- 0.3 to 4.1 +/- 0.4 L/min (p less than .001 for both). Cardiac index, stroke index, and left ventricular stroke work index were significantly increased. Pulmonary arterial and right atrial pressures, and systemic and pulmonary vascular resistances were also significantly reduced. Heart rate was not significantly altered. Mean systemic arterial pressure was slightly reduced. Flosequinan administration was not associated with symptomatic hypotension, cardiac arrhythmias, or other adverse events, and the hemodynamic effect was not related to the pretreatment serum sodium concentration. We conclude that flosequinan is effective in producing acute hemodynamic improvement in patients with heart failure complicating acute MI resistant to conventional therapy.

Administration, Oral↗
PubMed1989

Efficacy and safety of flosequinan, given over 3 days, evaluated by continuous hemodynamic monitoring.

The hemodynamic effects of flosequinan, a new balanced vasodilator, were evaluated in 12 patients with chronic congestive heart failure. The drug was added to diuretics and digitalis and given as an oral dose of 100 mg, once daily in the morning, over 3 days, and hemodynamic monitoring was performed before the first dose and for 72 h thereafter. Hemodynamic improvement, peaking between 1 and 2 h after oral administration, was observed on all 3 days. On day 1 pulmonary capillary wedge pressure (PCWP) was reduced from 27.8 +/- 8.6 to 13.0 +/- 3.1 mm Hg and cardiac output (CO) increased from 3.3 +/- 0.6 to 4.5 +/- 0.9 liters/min (p less than 0.05). After 12-16 h the effect was slightly attenuated but remained significant at 24 h. A similar response was observed after the doses given on days 2 and 3. At 72 h PCWP was 15.5 +/- 4.1 mm Hg and CO 3.8 +/- 1.1 liters/min (p less than 0.05 for the difference from baseline). Heart rate was slightly increased only at 2 h after the dose. Pulmonary arterial and right atrial pressure and systemic and pulmonary vascular resistances were significantly reduced (except for systemic resistance at 72 h). In conclusion, flosequinan produces hemodynamic improvement in patients with chronic congestive heart failure. The response to subsequent doses is similar to the response to the first dose.

Aged↗
PubMed1989

The effect of flosequinan in patients with acute-onset heart failure complicating acute myocardial infarction.

We studied the hemodynamic effect of a single dose of the new direct-acting vasodilator, flosequinan, in 25 patients with severe acute-onset heart failure complicating acute myocardial infarction, which was resistant to high doses of diuretics, nitrates and dobutamine given intravenously. Flosequinan was added to conventional therapy within 3.7 +/- 0.8 days of the infarction in the form of a single oral dose of 100 mg. Hemodynamic monitoring was performed every hour for 4 hours after the administration, without any other drug being added. Flosequinan produced hemodynamic improvement in all patients. The effect peaked at 1 to 2 hours and remained at this level at 4 hours. Pulmonary capillary wedge pressure decreased from 28.4 +/- 4.5 to 17.8 +/- 5.7 mmHg and cardiac output increased from 3.5 +/- 0.3 to 4.0 +/- 0.4 L/min (p less than 0.05 for both). Pulmonary arterial and pulmonary vascular resistances were also significantly reduced. Heart rate was not significantly altered. Mean systemic arterial pressure was slightly but not significantly reduced. Administration of flosequinan was not associated with symptomatic hypotension, cardiac arrhythmias or other adverse events and the hemodynamic effect was not related to the pre-treatment serum sodium concentration. We conclude that flosequinan is effective in producing acute hemodynamic improvement in patients with heart failure complicating acute myocardial infarction which is resistant to conventional therapy. Flosequinan is well tolerated in this group of patients and therefore further studies to determine the duration of action of the drug in this condition are appropriate.

Acute Disease↗
PubMed1989

The effect of cilazapril on systolic and diastolic cardiac function in hypertensive patients.

Diastolic function may be impaired in hypertensives even before alterations occur in systolic function. We studied the effect of a single dose of cilazapril, 5 mg orally, on systolic and diastolic cardiac function in 20 hypertensive patients using a double-blind crossover placebo controlled design. All patients had mild to moderate concentric left ventricular hypertrophy, preserved systolic function and long standing hypertension (for a period of 11.9 +/- 9.0 years). Radionuclide scintigraphy was performed with cilazapril and placebo, given one week apart. A two-week washout period of all cardioactive drugs preceded the study. Within one hour of oral administration of cilazapril blood pressure was significantly lowered. The absolute time to peak filling rate of the left ventricle, as well as the time to peak filling rate expressed as a percentage of diastole, were reduced from 176 +/- 34 to 158 +/- 33 msec (P less than 0.01) and from 46 +/- 10% to 37 +/- 8% (P less than 0.02) (reduction by 9% and 18.4%, respectively). Heart rate, left and right ventricular ejection fraction and peak filling rate was not significantly altered. Placebo had no significant effect. The effect of cilazapril is most probably related to afterload reduction. In conclusion; cilazapril seems to improve diastolic cardiac function in hypertensive patients. Long-term therapy may result in improvement of other, less sensitive indices of diastolic dysfunction.

Administration, Oral↗
PubMed1989

Radionuclide ventriculography and central aorta pressure change in noninvasive assessment of myocardial performance.

Systolic pressure-volume diagrams were obtained noninvasively by measuring the systolic central aortic pressure with a new device and by combining the pressure measurements, thus obtained, with absolute volume measurements obtained by radionuclide ventriculography during ejection. By dividing the peak power by the time elapsed from the beginning of ejection to the peak power point, the ejection rate of change of power (ERCP) was calculated. The ability of this index to assess left ventricular function at rest and exercise was evaluated in ten healthy subjects. ERCP proved to be more sensitive than global left ventricular ejection fraction increasing fivefold from rest to exercise compared with only 20% increase in global ejection fraction. ERCP increased dramatically postexercise from 3411 +/- 2173 to 18,162 +/- 14,633 gm/sec2, median 12,750, 95% confidence interval 9700-29,600, in healthy, while in patients it increased twofold from 2637 +/- 824 to 5062 +/- 1897 gm/sec2, median 4070, 95% confidence interval 2800-7030, p less than 0.001. ERCP had an excellent discriminative power in differentiating healthy subjects from patients, having 100% sensitivity, 90% specificity, 95% accuracy, 95% positive predictive value, and 90% negative predictive value. Thus, this noninvasive index seems to have a more comprehensive ability to evaluate changes in left ventricular function and shows a promising potential for clinical applications.

Adult↗
PubMed1988

Increased exercise tolerance and reduced duration of ischemia after isosorbide dinitrate oral spray in angina pectoris.

The prophylactic and therapeutic anti-ischemic efficacy of isosorbide dinitrate (ISDN) oral spray was assessed in 10 patients with coronary artery disease and stable angina pectoris. The patients entered a randomized crossover study of ISDN spray and placebo, involving bicycle exercise testing. Each patient underwent 2 exercise tests at least 4 hours apart. Immediately before initiation of exercise they received either ISDN spray or placebo and crossed over during the other test. ISDN spray delayed the onset of anginal pain by about 40%, from a mean of 5.1 +/- 1.4 minutes with placebo to 7.2 +/- 1.3 minutes with the active drug (p less than 0.001). Time of onset of ST-segment depression was also significantly prolonged, from 7.1 +/- 1.5 minutes with placebo to 10.2 +/- 1.2 minutes with ISDN (p less than 0.001). The patients achieved a higher double product at onset of pain with ISDN than with placebo. The drug also reduced the time of disappearance of pain after discontinuation of exercise from 3.2 +/- 0.7 to 2.1 +/- 0.8 minutes (p less than 0.001), and the time of disappearance of electrocardiographic changes from 4.2 +/- 0.6 to 2.5 +/- 0.8 minutes (p less than 0.005). These findings indicate that oral ISDN spray is an effective prophylactic for exercise-induced angina. Its rapid onset of action makes it especially suitable for usage immediately before exercise.

Administration, Oral↗
PubMed1988

Transdermal nitroglycerin patches for silent myocardial ischemia during antianginal treatment.

Because silent ischemia is not associated with an increase in heart rate and, being asymptomatic, its treatment requires constant therapeutic plasma levels of the drug used, a transdermal nitroglycerin patch (Deponit) was selected for treatment of this condition. Eight patients with documented silent ischemia were studied. All patients also had angina on effort treated with calcium antagonists (n = 8) and beta blockers (n = 6). They were evaluated by 24-hour ambulatory electrocardiographic monitoring. The transdermal nitroglycerin patch, 20 to 30 mg/24 hours, reduced the number of silent ischemic episodes from 9.25 +/- 5.52 to 2.4 +/- 2.0 episodes per 24 hours (p less than 0.001). The maximal ST-segment depression was reduced from 3.1 +/- 0.7 to 0.9 +/- 0.7 mm (p less than 0.001). Ventricular premature beats were significantly reduced, by 50%. Symptomatic ischemic episodes were completely suppressed. Thus, transdermal nitroglycerin, in moderate doses, is effective in suppressing silent ischemia in patients with angina pectoris who have silent ischemic episodes despite treatment with other antianginal agents.

Administration, Cutaneous↗