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Biomedical subjects

J Gottdiener

Publications and source records attributed to J Gottdiener.

8 recordsLinked to original sources
PubMed1989

Limitations of cough in maintaining blood flow during asystole: assessment by two-dimensional and Doppler echocardiography.

It has been previously demonstrated that patients can maintain consciousness by vigorously coughing during episodes of prolonged ventricular asystole or ventricular fibrillation. Using two-dimensional Doppler echocardiography and arterial blood pressure recordings, we evaluated the changes that occur during coughing in nine patients who were dependent on pacemakers and in whom periods of asystole could be induced. During asystole in each patient the mitral valve stayed partially open and the left ventricular area comprised 87% and 90% (apical four-chamber view, short-axis view, respectively) of the area during diastole of paced rhythm. Peak arterial pressure during coughing and asystole was 80% of peak systolic pressure of paced rhythm (P = 0.001). Left ventricular area during coughing was 110% (both apical four-chamber view and short-axis views) of the area during asystole when patients were not coughing. Both the mitral and aortic valves showed no appreciable motion during coughing. During coughing the mean flow velocity across the mitral valve was 0.06 +/- 0.03 m/sec and the flow velocity integral was 0.03 +/- 0.02 cm. Thus coughing during asystole produced minimal flow despite a rise in brachial arterial pressure.

Aged↗
PubMed1988

Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest.

The efficacy and safety of sotalol were assessed by electrophysiologic testing and ambulatory recordings in 16 patients with recurrent sustained ventricular tachycardia (VT) or nonfatal cardiac arrest who were refractory to an average of 4.8 conventional antiarrhythmic agents. Twenty-four-hour ambulatory recordings were performed before and after sotalol therapy. Fourteen patients underwent baseline electrophysiologic study and sustained VT was inducible in 12. Oral sotalol (320 to 960 mg/day) completely suppressed inducible sustained VT in 7 patients (58%), with modification in 3 (25%). Ventricular premature complexes were suppressed from baseline (mean +/- standard deviation) 431 +/- 616 to 60 +/- 110/hr (p less than 0.03). After a mean follow-up of 19 +/- 7 months, 12 of 14 patients receiving sotalol treatment had successful suppression of ventricular premature complexes (60 +/- 85/hr) and remained clinically free of sustained VT, except 2 who needed additional antiarrhythmic drugs to suppress the recurrent sustained VT. One patient died suddenly after 25 months of sotalol treatment. No severe side effects were noted during sotalol therapy. This study demonstrates that sotalol is a well-tolerated, effective antiarrhythmic agent in patients at high-risk for sudden death. It appears to be beneficial in patients who did not benefit from multiple drug treatment.

Adult↗
PubMed1985

Effect of diuretic therapy on ventricular arrhythmias in hypertensive patients with or without left ventricular hypertrophy.

Recent studies have suggested that hypertensive patients with ECG evidence of left ventricular hypertrophy (LVH) may have increased risk of sudden death when treated with diuretics. In the present study echocardiography was used as a more sensitive index for the presence of LVH. Thirty-one patients with uncomplicated hypertension underwent 48-hour ambulatory ECG monitoring both before any treatment and after 4 weeks of hydrochlorothiazide, (HCTZ), 100 mg daily. In 18 patients with left ventricular posterior wall thickness (LVPWT) greater than or equal to 13 mm (average = 14.4 +/- 0.2 mm) on echocardiogram, plasma potassium decreased from 4.1 +/- 0.3 to 3.3 +/- 0.4 mEq/L with HCTZ (p less than 0.01). Premature ventricular contractions (PVCs) averaged 5.7 +/- 9.9/hr at baseline and 7.1 +/- 16.6/hr following HCTZ (p = NS). The total number of couplets was 29 before and 13 after HCTZ, while four brief runs of ventricular tachycardia occurred only before treatment. In the remaining 13 patients with LVPWT less than or equal to 12 mm (average = 11.2 +/- 0.1 mm), plasma potassium decreased from 4.1 +/- 0.3 to 3.4 +/- 0.5 mEq/L with HCTZ (p less than 0.01). The average number of PVCs was 4.3 +/- 8.0/hr after HCTZ (p = NS). One couplet and one 3-beat run of ventricular tachycardia occurred before and one 3-beat run of ventricular tachycardia after HCTZ. Although more complex arrhythmias were noted in the LVH group, the differences were not statistically significant. These results indicate that thiazide therapy does not increase ventricular arrhythmias either in patients with or without LVH.

Adult↗
PubMed1982

Atrioventricular valve replacement in the idiopathic hypereosinophilic syndrome.

Three patients with the idiopathic hypereosinophilic syndrome and the associated endocardiopathy are described who underwent atrioventricular valve replacement after intractable congestive heart failure secondary to valvular dysfunction developed. Following valve replacement, all three patients sustained striking improvement in exercise tolerance and control of congestive heart failure. Thus, atrioventricular valve replacement may be beneficial to selected patients with congestive heart failure associated with the endocardial process of the idiopathic hypereosinophilic syndrome.

Adult↗
PubMed1980

Effect of therapy on left ventricular function in hypertension.

1. Twelve untreated hypertensive patients whose blood pressure was 171.8 +/- 5.5 mmHg systolic and 119.7 +/- 3.4 mmHg diastolic (mean +/- SEM) were treated aggressively with diuretics plus other antihypertensive agents. Echocardiograms were performed before, and 2 weeks, 3 months and 6 months after therapy. Blood pressures were lowered to an average of 142/98 mmHg over the 6 month period. 2. Mean velocity of circumferential fibre shortening rose from 1.1 +/- 0.09 to 1.3 +/- 0.06 diameters/s at 2 weeks and remained elevated at the end of 3 months (1.3 +/- 0.03 diameters/s) (P < 0.025), but returned to the control level in 6 months. Similarly, ejection fraction increased significantly during the same period from a control value of 65.1 +/- 4.4 to 73.4 +/- 1.8% (P < 0.025) and persisted in this range at 3 months. At 6 months the ejection fraction had returned to pretreatment levels. There were significant reductions in left ventricular end-systolic and end-diastolic dimensions. Left ventricular mass index decreased from 182.3 +/- 18.3 to 163.8 +/- 12.4 g/m2 after 6 months of therapy. 3. These results indicate that in the early stages of blood pressure reduction there is a temporary increase in ejection phase indices, probably related to afterload reduction. The reduction in the left ventricular mass index suggests that increased cardiac muscle mass due to elevated blood pressure may be partially reversible after long-term reduction in blood pressure.

Adult↗