PubMed Health⌕ Search

Biomedical subjects

R M Gunnar

Publications and source records attributed to R M Gunnar.

At least 19 recordsLinked to original sources
PubMed1992

The use of beta-blockade therapy in treatment of congestive heart failure.

If the activation of the sympathetic nervous system in chronic heart failure is causally related to progressive pump dysfunction, sudden death, and exercise intolerance, then selective blockade of the beta-adrenergic system may prove to be therapeutically beneficial. This report briefly reviews the evidence that there is systemic activation of the sympathetic nervous system in chronic heart failure, postulates mechanisms by which this activation might contribute to the morbidity and mortality of the syndrome, and hypothesizes further regarding how beta blockade may be beneficial in heart failure. The clinical evidence that the use of beta blockers is beneficial in the treatment of chronic heart failure is reviewed.

Adrenergic beta-Antagonists↗
PubMed1990

Progression of native coronary artery disease at 10 years: insights from a randomized study of medical versus surgical therapy for angina.

Repeat coronary angiography was performed in 42 patients 10 years after randomization to medical (n = 21) or surgical (n = 21) therapy for chronic angina. The native coronary arteries were classified into 15 angiographic segments and 3 arterial trunks for analysis of progression of coronary artery disease. The incidence rate of disease progression in coronary segments was 24% and 28% in medically and surgically treated patients, respectively (p = NS). Grafted segments showed a 38% rate of disease progression, which was higher than the 18% rate of for nongrafted segments (p less than 0.001) and the overall rate of 24% for medically treated patients (p less than 0.01). Similarly, 29 (94%) of 31 grafted arteries exhibited disease progression compared with 19 (59%) of 32 nongrafted arteries (p less than 0.01) and 42 (67%) of 63 arteries in medically treated patients (p less than 0.01). In grafted vessels, disease progression occurred more often in arteries proximal (84%) to the anastomosis than in arteries distal (16%) to graft insertion (p less than 0.001). Progression occurred in 46% of proximal segments compared with 23% of distal segments (p less than 0.02). Progression was seen in 23 (55%) of 43 segments with an occluded graft compared with 30 (31%) of 96 segments with a patent graft (p less than 0.02). Ten years after randomization, medically and surgically treated patients showed a comparable rate of disease progression in coronary segments. However, surgical therapy appeared to significantly accelerate atherosclerotic progression in the grafted vessels, especially in the proximal portions. Occluded grafts also correlated with an adverse effect on disease progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1987

Multivariate discriminant analysis of risk factors for operative mortality following isolated coronary artery bypass graft. Loyola University Medical Center experience, 1970 to 1984.

The Loyola Open-Heart Registry is a fully operational database that contains detailed data on approximately 9,000 patients who have undergone coronary bypass or cardiac valve replacement from January 1970 to December 1984. We analyzed the registry data using multivariate discriminant analysis to identify and quantitate those factors that might predict operative mortality (OM) for patients undergoing coronary artery bypass grafts at Loyola University Medical Center: Operative mortality was defined as death within 30 days following surgery. A total of 50 clinical and angiographic variables were analyzed for possible univariate association with operative mortality. Twenty-two variables were found to have significant univariate association with OM, and these 22 variables were subjected to multivariate discriminant analysis. For patients undergoing isolated, elective coronary artery bypass, the factors found to be predictive of OM are age (greater than 70) (F = 11.57), severe (more than six stenoses) coronary artery disease (F = 5.81), diffuse disease (F = 5.54), positive family history (F = 5.17), and number of coronary arteries bypassed (F = 4.78).

Coronary Artery Bypass↗
PubMed1986

Peripartum cardiomyopathy: clinical, hemodynamic, histologic and prognostic characteristics.

Peripartum cardiomyopathy is defined as left ventricular dilation and failure, first developing during the third trimester of pregnancy or in the first 6 months postpartum. In an effort to characterize this syndrome in a middle class population, 14 consecutive patients with peripartum cardiomyopathy underwent a detailed history and physical examination, right heart catheterization, M-mode and two-dimensional echocardiography, radionuclide ventriculography and right ventricular endomyocardial biopsy. These patients were then observed with sequential noninvasive studies to determine prognostic indicators. Eight (57%) of these 14 patients were primiparous and an equal number first presented with heart failure concomitant with or immediately before the onset of labor. When these women were compared with 55 patients with idiopathic dilated cardiomyopathy, only mean age at onset of symptoms (28.7 +/- 5.7 versus 48.2 +/- 13.6 years, p less than 0.001) and symptom duration (4.1 +/- 7.7 versus 19.0 +/- 18.4 months, p less than 0.001) differed between the groups. There was no difference in ventricular arrhythmia, left ventricular chamber size, ejection fraction or hemodynamics. Myocyte histologic findings were similar; however, myocarditis was identified in 29% of patients with peripartum cardiomyopathy and in only 9% of those with idiopathic dilated cardiomyopathy. In all patients with peripartum cardiomyopathy and myocarditis, the myocardial biopsy was performed within 1 week of onset of symptoms. Seven (50%) of the patients with peripartum cardiomyopathy had dramatic improvement within 6 weeks of follow-up, and 6 (43%) died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Clinical aspects of virus/immune myocarditis.

Although a cause-and-effect relationship between viral infection and myocarditis remains inferential, two distinct clinical syndromes can be identified. During the early viral phase, the cardiac manifestations emerge while the symptoms of active viral infection are also present. During the chronic phase, symptoms of the viral infection may be remote or nonexistent, and identification of active myocarditis is contingent upon an aggressive diagnostic approach with endomyocardial biopsy and gallium 67 imaging. The exact incidence of myocarditis in patients with heart failure of unknown cause is unclear due to lack of standardization of histologic parameters. There are no other clinical clues to the presence of myocarditis in those patients presenting with cardiomyopathy or ventricular arrhythmia. For further clarification of the incidence and various presentations of myocarditis a large multi-center trial is necessary.

Acute Disease↗
PubMed1985

Ventricular fibrillation during coronary angiography: an analysis of mechanisms.

To investigate the mechanisms of ventricular fibrillation (VF) during coronary angiography, we assessed ventricular automaticity, local QT intervals, local conduction characteristics, and the ability to induce arrhythmias with premature ventricular stimulation in 30 dogs after intracoronary injections of 4 to 6 cc of Renografin 76 (RG 76). Ventricular automaticity was measured in six dogs as the idioventricular escape rate following intense vagal stimulation and was unchanged (51 +/- 6 vs 52 +/- 6 bpm, p greater than 0.05) with 6 cc of RG 76. In addition, 8 of 10 injections of 6 cc of RG 76 produced VF at a heart rate of 200 bpm compared to only 2 of 10 injections at a heart rate of 80 bpm (p less than 0.05). Composite and bipolar plunge electrodes were placed in the region perfused by the left anterior descending coronary artery (LAD) and circumflex coronary artery to assess QT intervals and conduction characteristics. RG 76, 4cc, produced a 116 +/- 18 msec increase in the QT intervals recorded from the region perfused by the LAD, resulting in a marked dispersion in repolarization. Both local bipolar and composite electrograms showed minimal conduction delay, which rarely extended beyond the QRS of a lead II ECG during atrial paced rhythm. As premature beats (spontaneous or induced) conducted through the region of QT prolongation, marked conduction delay was recorded from bipolar electrograms, while composite electrograms recorded continuous fractionated electrical activity spanning the diastolic interval at the onset of VF.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗