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Biomedical subjects

D V Unverferth

Publications and source records attributed to D V Unverferth.

At least 91 records · Page 5Linked to original sources
PubMed1983

Human myocardial histologic characteristics in congestive heart failure.

The purpose of this study was to identify the histologic characteristics of human myocardium in congestive heart failure (CHF) by cellular hypertrophy, nuclear area, endocardial thickness, and percentage of fibrosis and to correlate histologic findings to cause, severity, and duration of disease. Right ventricular endomyocardial biopsies from 109 patients were quantitatively analyzed. Ten patients with normal cardiac history, physical examination results, and cardiac function served as the control group. The remaining patients were divided into the following groups: those treated with doxorubicin (n = 18), and those with chest pain with normal coronary arteries (n = 8), familial CHF (n = 3), CHF associated with myotonic dystrophy (n = 3), peripartal CHF (n = 2), valvular CHF (n = 9), alcohol-induced CHF (n = 13), postviral CHF (n = 6), or idiopathic CHF (n = 36). Linear regression analyses showed a strong correlation between cell diameter and nuclear area (r = .70, p less than .001) and weaker correlations between amount of fibrosis and cell diameter (r = .30, p less than .005) and fibrosis and nuclear area (r = .29, p less than .005). Results of function studies and histologic measurements (e.g., echocardiographically measured change in the minor-axis dimension of the left ventricle with systole and cell diameter) correlated poorly (r = -.33, p less than .005). Duration of dyspnea did not correlate with any histologic factor. Within the normal group there was a direct correlation of cell diameter with age (r = .67, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1983

Drugs five years later. Dobutamine.

Dobutamine is a synthetic catecholamine developed as a relatively selective positive inotropic drug for short-term parenteral administration. Dobutamine's effects are mediated by strong beta 1 adrenergic receptor stimulation and mild stimulation of beta 2 and alpha 1 receptors. Dobutamine should be used to improve ventricular function and cardiac performance in patients in whom ventricular dysfunction has caused a reduced stroke volume and cardiac output, a mild to moderate drop in systemic blood pressure, diminished organ and tissue perfusion, and elevated ventricular filling pressures. When guidelines for patient selection and dosing are adhered to, ventricular dysfunction and cardiac decompensation secondary to atherosclerotic occlusive coronary artery disease can be improved without adversely affecting the myocardial oxygen supply and demand balance. Dobutamine has less vasopressor activity than norepinephrine and dopamine, and should not be the primary treatment in conditions characterized by marked hypotension and shock.

Animals↗
PubMed1983

Attempt to prevent doxorubicin-induced acute human myocardial morphologic damage with acetylcysteine.

Doxorubicin induced acute as well as chronic myocardial morphologic alterations. Twenty patients with normal cardiovascular function were randomized to 2 groups based on age and dose of doxorubicin. Group I received placebo 1 hour before doxorubicin administration; group II received acetylcysteine (N-acetyl-L-cysteine) (Nac) 1 hour before doxorubicin. Endomyocardial biopsies were performed at base line at 4 and 24 hours after doxorubicin administration. Biopsy tissue was viewed by electron microscopy, and stereoscopic techniques were used to determine tubular and mitochondrial area. The change of the tubular area was similar in the 2 groups, was maximum at 4 hours, and was proportionately spread throughout the cell. The mitochondrial swelling was also similar in the 2 groups and proportionate throughout the cell but was maximum at 24 hours. This study demonstrated that the acute doxorubicin-induced damage was diffuse and not prevented by Nac.

Acetylcysteine↗
PubMed1983

Acute and chronic isosorbide dinitrate therapy in congestive heart failure: demonstration of improved exercise capacity and differing arterial and venous tolerance during chronic administration.

Thirty patients with congestive heart failure underwent a double-blind study after randomization into either isosorbide dinitrate or placebo. The initial dose (40 mg orally) of isosorbide dinitrate reduced resting and exercise pulmonary artery, pulmonary capillary wedge, and systemic blood pressure and pulmonary and systemic vascular resistance without improving exercise tolerance. Chronic dosing (40 mg orally every 6 h for 3 months) increased exercise tolerance and maintained a reduction in resting and exercise pulmonary artery and pulmonary capillary wedge pressures and pulmonary resistance, while systemic pressure and resistance returned to baseline. Chronic oral isosorbide dinitrate (40 mg every 6 h) improves exercise capacity over a 3-month period with disparate tolerance effects on systemic arterial, systemic venous, and pulmonary vasculature.

Heart Failure↗
PubMed1983

Cardiac evaluation of mitoxantrone.

Mitoxantrone is a synthetic anthraquinone that was developed through the doxorubicin analog program in hopes of retaining anticancer activity with less cardiotoxicity. This study evaluated 18 patients receiving mitoxantrone with serial noninvasive tests of left ventricular function and with endomyocardial biopsy. The echocardiograms and systolic time intervals demonstrated a trend to deterioration that did not achieve statistical significance. However, the nuclear angiographic ejection fraction significantly decreased from 61% +/- 6% (means +/- SD) at baseline to 58% +/- 5% (P less than 0.05) after 48 mg/m2 of mitoxantrone. The endomyocardial biopsies revealed tubular swelling, degeneration of mitochondria, minimal chromatin clumping, and myofibrillar lysis. This study has revealed mild but definite impairment of cardiac function and mild changes of myocardial morphology during mitoxantrone therapy. Although mitoxantrone is an effective chemotherapeutic agent, a direct comparison of mitoxantrone with doxorubicin is necessary to compare relative therapeutic to cardiotoxic ratios.

Aged↗
PubMed1983

Heart rate responsiveness after sustained chronotropic stimulation with a beta 1-adrenergic receptor agonist.

Six normal male human subjects underwent two 72 hr infusions of saline (control) and butopamine, a beta-adrenergic agonist with strong positive chronotropic properties, in order to determine the chronotropic responsiveness of the human heart after sustained chronotropic stimulation. Chronotropic responsiveness was assessed by heart rate responses to intravenous isoproterenol and bicycle ergometry before and serially over 50 hr after discontinuation of the infusions. Chronotropic responsiveness to isoproterenol and exercise was reduced significantly in the butopamine group compared to control; this blunted chronotropic effect persisted beyond 48 hr. Positive inotropic responsiveness, assessed by echocardiography and systolic time intervals, was reduced modestly for the butopamine-treated group up to 24 hr after infusion. Although the precise mechanisms are not fully elucidated, continuous chronotropic stimulation of the human heart with the beta 1 agonist, butopamine, elicits a significant reduction in the heart rate response to isoproterenol and exercise challenges. In addition, the degree and time course of suppression of the chronotropic vs. inotropic responsiveness are disparate.

2-Hydroxyphenethylamine↗
PubMed1982

Cardiac function in Duchenne's muscular dystrophy. Results of 10-year follow-up study and noninvasive tests.

The purposes of this study were to: (1) evaluate the progression of cardiac involvement in Duchenne's muscular dystrophy using systolic time intervals (PEP/LVET); (2) determine if the degree of cardiac involvement bears a relation to the severity of skeletal muscle disease; and (3) describe the M-mode and two-dimensional echocardiographic findings. In 1970, systolic time intervals were studied in 16 patients. During the 10-year interim, two patients were lost to follow-up study, and five patients died. Nine remaining patients were re-studied in 1980 with M-mode and two-dimensional echocardiography as well as systolic time intervals. The PEP/LVET value of these nine patients increased from 0.37 +/- 0.05 (mean +/- SD) in 1970 to 0.47 +/- 0.07 (p less than 0.005) in 1980. Three patients remained ambulatory, and their PEP/LVET value (0.41 +/- 0.04) was significantly better than that of the nonambulatory patients (0.50 +/- 0.07, p less than 0.05). The M-mode echocardiography percentage diameter change was also worse in the nonambulatory group (21 +/- 4 percent versus 34 +/- 7 percent, p less than 0.02). The five patients who were nonambulatory in 1970 died in the intervening 10 years. This study demonstrated that the heart disease of Duchenne's muscular dystrophy is progressive and that the severity of skeletal muscle disease is probably associated with the degree of cardiac dysfunction.

Adolescent↗
PubMed1982

The pattern of myocardial degeneration in nonischemic congestive cardiomyopathy.

The histopathologic features of nonischemic congestive cardiomyopathy (CCM) include diffuse and focal fibrosis, vacuolar degeneration, and myofiber hypertrophy. Eleven patients with CCM and five controls were studied. Fibrosis and degree of vacuolization were quantified by means of stereologic techniques; myocardial cell diameter was measured with an ocular micrometer. Five levels of the left ventricular free wall were examined. Area I was immediately subepicardial, and area 5 was immediately subendocardial. In all areas, fibrosis, vacuolization, and fiber diameter were significantly greater in the experimental group than in the control group (P less than 0.05). In addition, fibrosis and vacuolization had an umbrella distribution, which peaked in area 4, the area adjacent to the subendocardium (P less than 0.01). The distributions of fibrosis and vacuolar degeneration suggest compromised blood flow to the inner myocardial layers, with relative sparing of the immediate subendocardial region owing to its proximity to the left ventricular cavity.

Adult↗
PubMed1982

Effects of hydralazine on coronary blood flow and myocardial energetics in congestive heart failure.

The acute effects of oral hydralazine, 1 mg/kg, on coronary vascular resistance, coronary blood flow (estimated using the coronary sinus thermodilution technique), and myocardial oxygen consumption were evaluated in 10 patients with chronic (New York Heart Association class III and IV) nonischemic congestive heart failure. Central hemodynamic responses demonstrated a modest decrease in mean arterial pressure, pulmonary capillary wedge pressure and systemic vascular resistance (12%, 15% and 29%, respectively), while the cardiac index increased from 2.3 +/- 0.1 to 3.1 +/- 0.3 and left ventricular stroke work index from 24 +/- 3.7 to 28 +/- 3.4 (p less than 0.01). Heart rate and diastolic filling time did not change. Coronary blood flow increased approximately 50%, from 144 +/- 17 to 218 +/- 30 ml/min, and coronary vascular resistance decreased from 0.55 +/- 0.09 to 0.36 +/- 0.08 mm Hg/ml/min (both p less than 0.01). Oral hydralazine increased myocardial oxygen consumption by 33%, from 15 +/- 1.6 to 20 +/- 2.7 ml/min. Despite this moderate augmentation in myocardial oxygen consumption, the arterial-coronary sinus oxygen difference decreased from 104 +/- 6.2 to 94 +/- 7.5 and the myocardial oxygen extraction ratio decreased from 71% to 64% (both p less than 0.05). The ratio of coronary vascular resistance to systemic vascular resistance decreased with hydralazine therapy, while coronary blood flow increased from 3.5% to 4.3 % of total cardiac output. In this group of patients with nonischemic cardiomyopathy, hydralazine had a favorable effect on the coronary circulation and improved the critical myocardial oxygen supply-demand ratio.

Adult↗
PubMed1982

Drug-induced conditioning in congestive heart failure.

Continuous 72-hour infusions of dobutamine reportedly effect sustained clinical improvement in patients with congestive heart failure. This study was designed to determine if shorter, more frequent infusions, delivered in an outpatient setting, elicit a similar response. Twenty-six patients with moderately severe congestive heart failure were randomized, 11 into a control group and 15 into a dobutamine treatment group. Baseline data were collected for 4 weeks in each group. Thereafter, the dobutamine treatment group received 4-hour infusions of dobutamine weekly for 24 weeks. Systolic time intervals, echocardiography, cardiac index and treadmill exercise tolerance were used to follow the progress of the control and dobutamine treatment groups. The ratio of preejection period to left ventricular ejection time and the cardiac index did not change significantly in either group. The velocity of circumferential fiber shortening and the percent change in the minor axis of the left ventricle during systole improved modestly (p less than 0.05) above baseline in the dobutamine group after 14 weeks of treatment and above the corresponding control values (p less than 0.05) after 22 weeks. Exercise tolerance (duration) improved 25--51% (all p less than 0.05) above baseline in the dobutamine group compared with 10--17% (all p greater than 0.05 vs baseline) in the control group. Heart rate at maximal exercise did not change significantly from baseline for either group and did not differ significantly between the two groups. Functional classification improved in 12 of 15 dobutamine treatment patients and in only two of 11 control patients (p less than 0.05). In our patients with congestive heart failure, weekly 4-hour dobutamine infusions did not elicit a major change in resting left ventricular function; however, exercise performance and clinical status improved considerably.

Adult↗
PubMed1982

The effect of vasodilator therapy on systolic and diastolic time intervals in congestive heart failure.

To determine the effects of vasodilator drugs on systolic and diastolic time intervals in patients with congestive heart failure, these noninvasive measurements were made in 50 patients with moderately severe disease before and after vasodilator therapy. These data were compared with direct hemodynamic measurements obtained simultaneously from a flow-directed triple-lumen pulmonary artery catheter placed in each patient. Oral vasodilators included isosorbide dinitrate 20 mg (n-8), hydralazine 75 mg (n-8), and 100 mg (n-8), and first-dose prazosin 2 mg (n-8) and 5 mg (n-8). Ten additional patients received intravenous dose-response infusions of isosorbide dinitrate, nitroglycerin, and nitroprusside. Increases in cardiac output and stroke volume effected a decrease (improvement) in the systolic time interval parameter of ventricular performance, PEP/LVET. The correlation coefficient for vasodilator-induced changes in cardiac output vs changes in PEP/LVET was -0.82 (P less than 0.05) and for changes in stroke volume and PEP/LVET was -0.75 (P less than 0.05). In general, the diastolic time period was not significantly affected by these drugs. The systolic time intervals are a simple and useful method for evaluation of vasodilator therapy in patients with congestive heart failure.

Administration, Oral↗
PubMed1982

Vasodilators and prostaglandin inhibitors in primary pulmonary hypertension.

Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

Adolescent↗