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Dive into the research topics where Ronald M. Rossen is active.

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Featured researches published by Ronald M. Rossen.


Circulation | 1974

Effect of Nitroprusside on Left Ventricular Dynamics in Mitral Regurgitation

Daniel J. Goodman; Ronald M. Rossen; Earl L. Holloway; Edwin L. Alderman; Donald C. Harrison

In order to evaluate the circulatory action of vasodilator therapy in patients with significant mitral regurgitation, sodium nitroprusside was infused intravenously in 14 patients who had mitral regurgitation due to a variety of causes. In 13 of these patients, valvular insufficiency had been present for several years. The mean arterial pressure fall from 88 ± 1.2 to 71 ± 2.1 mm Hg was accompanied by a significant decrease in pulmonary artery pressure (from 27.4 ± 2.7 to 19.1 ± 2.4 mm Hg), pulmonary artery wedge v wave (from 31.7 ± 3.3 to 17.0 ± 1.9 mm Hg), and left ventricular end-diastolic pressure (from 16.7 ± 1.6 to 9.3 ± 1.2 mm Hg). In 10 patients significant decreases in angiographic end-diastolic volumes (from 196 ± 10 to 177 ± 10 ml) and end-systolic volumes (from 90 ± 10 to 77 ± 9 ml) were accompanied by slight decreases in the total stroke volume and slight increases in the ejection fraction. The improved forward stroke volume index (from 27 ± 3.0 to 33 ± 2.1 ml) was due to a very significant reduction in the regurgitant fraction (from 57 ± 6 to 42 ± 6%). Nitroprusside, therefore, has beneficial hemodynamic effects in patients with chronic mitral regurgitation.


Circulation | 1974

Echocardiographic Criteria in the Diagnosis of Idiopathic Hypertrophic Subaortic Stenosis

Ronald M. Rossen; Daniel J. Goodman; Robert E. Ingham; Richard L. Popp

Echocardiography has proven to be a useful technique in the diagnosis and assessment of therapy in idiopathic hypertrophic subaortic stenosis (IHSS). Asymmetric septal hypertrophy has been described as the pathognomonic anatomic marker of the disease. A characteristic systolic anterior motion of the anterior mitral valve leaflet has been detected in the presence of hemodynamically significant subaortic left ventricular outflow obstruction. An echocardiographic quantification of the outflow gradient (the obstruction index) has been derived previously.Four patients were studied by ultrasound at the time of cardiac catheterization. All four demonstrated systolic anterior motion of the anterior mitral leaflet in the absence of a resting gradient. In three of the four, the calculated obstruction index predicted hemodynamically significant resting gradients. All four patients were shown to have labile gradients with provocative maneuvers. A fifth patient with abnormal systolic anterior motion demonstrated a close correlation between the obstruction index and resting gradient; however, symmetric hypertrophy of the septum and left ventricular posterior wall was detected by ultrasound. Therefore, the abnormal mitral valve pattern may be seen in the absence of a resting gradient and symmetric left ventricular hypertrophy may exist in the presence of IHSS.


Circulation | 1975

Effect of digoxin on atioventricular conduction. Studies in patients with and without cardiac autonomic innervation.

Daniel J. Goodman; Ronald M. Rossen; David S. Cannom; Alan K. Rider; Donald C. Harrison

The effect of digoxin on atrioventricular (a-v) conduction was compared in five patients with an intact cardiac autonomic nervous system (Group I) and seven patients who had undergone cardiac transplantation (Group II), in whom we have previously shown the transplanted heart to be completely denervated. Small decreases in the atrial effective refractory period (ERP) (from 262 plus or minus 12 to 254 plus or minus 11 msec) and atrial functional refractory period (FRP) (from 304 plus or minus 12 msec) were observed in Group I patients after digoxin, but these changes were not significant. However, significant increases in the A-V nodal ERP (from 315 plus or minus 18 msec to 351 plus or minus 17 msec, P less than 0.05), and A-V nodal FRP (from 426 plus or minus 42 to 460 plus or minus 46 msec, P less than 0.01) were produced by digoxin and were unrelated to changes in cycle length. In Group II patients with denervated hearts, changes in atrial ERP (from 246 plus or minus 4 to 243 plus or minus 6 during spontaneous sinus rhythm; from 204 plus or minus 10 to 216 plus or minus 8 msec during atrial pacing) and atrial FRP (from 311 plus or minus 12 to 316 plus or minus 11 msec during spontaneous sinus rhythm; from 254 plus or minus 12 to 260 plus or minus 10 msec during atrial pacing) were not significant. However, in contrast to the Group I patients, the digoxin-induced changes in A-V nodal ERP (from 280 plus or minus 22 to 297 plus or minus 18 msec during atrial pacing) and FRP (from 368 plus or minus 18 to 377 plus or minus 18 msec during spontaneous sinus rhythm; from 334 plus or minus 13 to 346 plus or minus 16 msec during atrial pacing) were also statistically insignificant. Our results demonstrate that the electrophysiologic effects of digoxin on atrioventricular conduction in man are most marked in the atrioventricular node and are dependent on cardiac innervation


The New England Journal of Medicine | 1974

Ventricular Systolic Septal Thickening and Excursion in Idiopathic Hypertrophic Subaortic Stenosis

Ronald M. Rossen; Daniel J. Goodman; Robert E. Ingham; Richard L. Popp

Abstract Asymmetric septal hypertrophy has been described as the pathognomonic abnormality in idiopathic hypertrophic subaortic stenosis. It has been suggested that the ventricular septum is hyperc...


American Journal of Cardiology | 1978

Electrophysiologic Findings in Patients With Idiopathic Hypertrophic Subaortic Stenosis

Robert E. Ingham; Jay W. Mason; Ronald M. Rossen; Daniel J. Goodman; Donald C. Harrison

Thirteen patients with catheterization-proved idiopathic hypertrophic subaortic stenosis underwent intracardiac electrophysiologic study. There was a large incidence of arrhythmias and a strikingly large incidence of conduction system abnormalities among these patients. The P-A and A-H intervals were normal in all patients. Atrial pacing resulted in Mobitz type 1 block proximal to the His bundle at an abnormal rate (less than 140/min) in 2 of 12 patients (17 percent). H-V intervals were prolonged (greater than 50 msec) in 10 of 12 patients (83 percent) and were greater than 60 msec in 7 patients (58 percent). The atrial effective refractory period was prolonged in 3 of 12 patients and was markedly prolonged in 1 of them. Effective refractory period of the atrioventricular (A-V) node, determined in five patients, was prolonged in three. Dual responses of the A-V node to atrial extrastimuli were found in seven patients. Dual A-V nodal repsonses were evoked with propranolol in three patients and persisted in the other four patients with dual responses despite propranolol administration.


American Heart Journal | 1976

The effect of cycle length on cardiac refractory periods in the denervated human heart

Daniel J. Goodman; Ronald M. Rossen; Alan K. Rider; Donald C. Harrison

We have previously demonstrated that the transplanted human heart is functionally denervated. With the use of the extra stimulus technique during His bundle electrocardiography, refractory periods of the arterioventricular (A-V) conduction system were determined at several heart rates after pacing-induced changes in cycle length in eight patients who had previously undergone cardiac transplantation. Shortening of the cycle length was accompanied by a decrease in both the effective and functional refractory periods of the atrium. No consistent change in A-V nodal effective refractory period or functional refractory period could be demonstrated. Because A-V conduction was limited at shorter cycle lengths by the functional refractory periods of the atrium and A-V node, bundle branch refractory periods could be determined in three patients only at the longest cycle length studied. In four of the eight patients, atrial arrhythmias were produced at short cycle lengths with the introduction of early atrial extra stimuli. This may be due to a lack of vagal innervation of the atrium. These results contribute to our understanding of atrial arrhythmias.


American Heart Journal | 1979

Echocardiographic diagnosis of pericardial disease.

Michael S. Horowitz; Ronald M. Rossen; Donald C. Harrison

Echocardiograms were performed in 11 patients with constrictive pericarditis or effusive-constrictive pericarditis confirmed by cardiac catheterization and pericardiectomy. Three echocardiographic patterns of pericardial disease were noted and were related to three types of pericardial pathology. Parallel moving echoes separated by a clear space were reflected from chronically fibrosed and thickened pericardium without associated pericardial exudate. Effusive-constrictive pericarditis or subacute wet pericarditis was characterized on the echocardiogram by a posterior echo-free space representing the liquid pericardial effusion and multiple ultrasonic lines from the thickened visceral pericardium. Subacute dry pericarditis was associated with numerous ultrasonic signals filling the space between the visceral pericardium and the relatively flat parietal pericardium. These ultrasonic signals were reflected from coagulated pericardial exudate which was adherent both to the parietal pericardium and the visceral pericardium. Parallel moving echoes or dense bands of echoes were reflected from either or both thickened visceral and parietal pericardium.


American Journal of Cardiology | 1975

Effect of digoxin on atrioventricular conduction: Studies in patients with and without cardiac autonomic innervation

Ronald M. Rossen; Daniel J. Goodman; David M. Cannom; Alan K. Rider; Donald C. Harrison

The effect of digoxin on atrioventricular (A-V) conduction was compared in five patients with an intact cardiac autonomic nervous system (Group I) and seven patients who had undergone cardiac transplantation (Group II), in whom we have previously shown the transplanted heart to be completely denervated. Small decreases in the atrial effective refractory period (ERP) (from 262 ± 12 to 254 ± 11 msec) and atrial functional refractory period (FRP) (from 304 ± 12 msec to 298 ± 12 msec) were observed in Group I patients after digoxin, but these changes were not significant. However, significant increases in the A-V nodal ERP (from 315 ± 18 msec to 351 ± 17 msec, P < 0.05), and A-V nodal FRP (from 426 ± 42 to 460 ± 46 msec, P < 0.01) were produced by digoxin and were unrelated to changes in cycle length. In Group II patients with denervated hearts, changes in atrial ERP (from 246 ± 4 to 243 ± 6 during spontaneous sinus rhythm; from 204 ± 10 to 216 ± 8 msec during atrial pacing) and atrial FRP (from 311 ± 12 to 316 ± 11 msec during spontaneous sinus rhythm; from 254 ± 12 to 260 ± 10 msec during atrial pacing) were not significant. However, in contrast to the Group I patients, the digoxin-induced changes in A-V nodal ERP (from 280 ± 22 to 297 ± 18 msec during atrial pacing) and FRP (from 368 ± 18 to 377 ± 18 msec during spontaneous sinus rhythm; from 334 ± 13 to 346 ± 16 msec during atrial pacing) were also statistically insignificant. Our results demonstrate that the electrophysiologic effects of digoxin on atrioventricular conduction in man are most marked in the atrioventricular node and are dependent on cardiac innervation.


The American Journal of Medicine | 1975

A-V conduction disturbances in Reiter's syndrome

Ronald M. Rossen; Daniel J. Goodman; Donald C. Harrison

High grade atrioventricular (A-V) block is a rarely described complication of Reiters syndrome. This 65 year old man had recurrent episodes of arthritis, conjunctivitis and urethritis beginning at age 16. A prolonged P-R interval was first noted at age 32. The conduction distrubance progressed to intermittent episodes of high grade and complete heart block by age 65. His bundle electrograms located the site of block above the level of the bundle of His. Atrial pacing to rates of 150/min produced 5:1 A-V block, whereas exercise and atropine administration resulted in 1:1 A-V conduction. In view of these results, artificial pacemaker therapy is not indicated. The association of conduction disorders and Reiters syndrome is reviewed.


Chest | 1974

Echocardiographic Pseudo Idiopathic Hypertrophic Subaortic Stenosis

Daniel J. Goodman; Ronald M. Rossen; Richard L. Popp

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