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Biomedical subjects

S M Mohiuddin

Publications and source records attributed to S M Mohiuddin.

At least 55 records · Page 3Linked to original sources

Myocardial infarction after dipyridamole-assisted thallium-201 imaging.

A 77-year-old woman with suspected coronary artery disease underwent an oral dipyridamole/thallium-201 myocardial imaging study. Approximately 75 minutes after ingestion of dipyridamole 300 mg suspension, the patient developed chest pain, hypotension, nausea, and diaphoresis. An electrocardiogram revealed ST-T wave changes suggestive of inferior ischemia. Appropriate therapeutic measures, including aminophylline and nitroglycerin, were instituted. Delayed thallium images revealed reversible ischemia in the anteroseptal and posterobasal regions with a fixed defect in the inferobasal region. Cardiac enzyme studies were also indicative of acute myocardial injury. The patient subsequently underwent coronary arteriography and four-vessel coronary artery bypass grafting and was discharged without further complication. This report raises concerns about the potential danger of dipyridamole in patients with severe coronary artery stenosis and collateral circulation. Prophylactic aminophylline should be considered in these patients.

Aged↗

Nifedipine in the treatment of hypertensive episodes in the coronary care unit.

The effectiveness of nifedipine for the treatment of acute hypertensive episodes in patients already taking chronic calcium-channel blocker therapy is unknown. We report our experience with 43 consecutive patients who received nifedipine for acute hypertensive episodes in the coronary care unit. Of the 43 patients (24 men, 19 women), 23 (53 percent) were taking chronic (greater than 2 mo) calcium-channel blocker therapy. Nifedipine 10 mg capsules were chewed and swallowed with repeat doses given at hourly intervals if necessary. Target BP was 140/90 mm Hg, which was achieved in 31 of 43 patients (72 percent). In patients already taking calcium-channel blockers, target BP was achieved in 18 of 23 patients (78 percent). Response in patients not taking chronic calcium-channel blockers was observed in 13 of 20 patients (65 percent). Overall, adverse effects occurred in 16 of 43 patients (37 percent): 11 of 23 patients (48 percent) taking calcium-channel blockers, and 5 of 20 patients (25 percent) not taking calcium-channel blockers. Nifedipine is equally effective in lowering BP in patients taking calcium-channel blockers as it is in patients not taking them. Although associated with a higher incidence of adverse effects in patients already taking calcium-channel blockers, these effects were not considered serious. Nifedipine is an effective agent in acute hypertensive episodes, even in patients receiving chronic calcium-channel blocker therapy.

Adult↗

Crossover comparison of cibenzoline and quinidine in ambulatory patients with chronic ventricular arrhythmias.

This study was designed to compare the efficacy and safety of cibenzoline and quinidine in ambulatory patients with ventricular arrhythmias. Following washout of previous antiarrhythmic treatment, a 48-h ambulatory electrocardiographic (ECG) recording was obtained. Twenty-seven patients were screened, of whom 20 met the entry criteria of greater than or equal to 30 ventricular premature beats (VPBs)/h. Cibenzoline was started at 130 mg every 12 h and was increased to 160 mg every 12 h if necessary. Quinidine was started at 300 mg every 6 h and was increased to 400 mg every 6 h if necessary. Treatment was assessed by 24-h ambulatory ECG recording. Efficacy was defined as greater than 75% reduction in single VPBs, greater than 90% reduction in paired VPBs, and total abolition of ventricular tachycardia events. A 7-day washout with repeat 24-h ambulatory ECG recording to document return of ventricular arrhythmias was required prior to crossover. Efficacy was documented in 9 of 20 (45%) patients receiving cibenzoline and in 9 of 20 (45%) patients receiving quinidine. Response to cibenzoline 130 mg every 12 h was documented in 8 of 20 (40%) patients and in 1 of 11 (9%) patients receiving cibenzoline 160 mg every 12 h. Response to quinidine 300 mg every 6 h was documented in 8 of 20 (40%) patients and in 2 of 6 (33%) patients receiving 400 mg every 6 h. Dose-limiting side effects occurred in 1 of 20 (5%) patients receiving cibenzoline and in 7 of 20 (35%) patients receiving quinidine. Cibenzoline and quinidine are equal in efficacy, but cibenzoline is significantly better tolerated.

Adult↗

Efficacy and tolerance of tocainide during long-term treatment of malignant ventricular arrhythmias.

A group of 51 patients with malignant ventricular arrhythmias refractory to standard oral antiarrhythmic agents were treated with oral tocainide. Antiarrhythmic efficacy was defined as total abolition of occurrences of ventricular tachycardia (VT) or ventricular fibrillation (VF) as assessed by hospital admissions for arrhythmias and the occurrence of sudden cardiac death (SCD). Of the 51 patients, 32 (63%) initially tolerated tocainide and were discharged from the hospital. Of the 19 patients not initially responding to tocainide, 6 (12%) had arrhythmia recurrence and 13 (25%) developed intolerable central nervous system or gastrointestinal side effects. Of these 19 short-term nonresponders, 8 (42%) patients suffered SCD over an average follow-up of 24 months (annual SCD rate of 21%). Two patients suffered SCD during the first week of tocainide therapy. Discounting the 2 patients with SCD on tocainide therapy, 6 of 17 (35%) patients initially withdrawn from tocainide suffered SCD (annual SCD rate of 18%). Twenty-four of the 32 short-term responders did not have arrhythmia recurrence over a mean follow-up of 38 months resulting in an overall long-term efficacy of 47% (24/51). Over an average follow-up of 38 months for these 24 short-term responders, 12 patients expired from nonarrhythmic causes, 3 patients were withdrawn for non-drug-related causes, and 9 patients remain on tocainide therapy. Of the 8 long-term nonresponders, 3 patients had arrhythmia recurrence and died suddenly while 5 patients developed intolerable side effects. The annual SCD rate in short-term responders was 3%. Eighteen of the 51 patients (35%) were withdrawn from the study because of adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden↗

Double-blind randomized comparison of intravenous tocainide versus lidocaine in the treatment of chronic ventricular arrhythmias.

The efficacy and safety of intravenous tocainide were compared with intravenous lidocaine in patients with chronic ventricular arrhythmias in a double-blind, parallel study. Twenty-nine patients were randomized to a tocainide (n = 15) or lidocaine (n = 14) group. Antiarrhythmic efficacy was defined as a greater than or equal to 50% reduction in single ventricular premature complex (VPC) frequency, greater than or equal to 90% reduction in paired VPC frequency, and total abolition of ventricular tachycardia. Efficacy was observed in 40% (6 of 15) of patients in the tocainide group and in 36% (5 of 14) patients in the lidocaine group. A 75% or greater reduction in total VPCs occurred in 40% (6 of 15) of patients in the tocainide group and in 57% (8 of 14) of patients in the lidocaine group. Greater than 90% suppression of paired VPCs occurred in 9 of 13 (69%) patients taking tocainide and in 6 of 11 (54%) patients taking lidocaine. Total abolition of ventricular tachycardia was documented in 5 of 11 (45%) patients given tocainide and in two of six (33%) patients given lidocaine. A total of 17 adverse reactions affecting 86% (12 of 14) of patients taking lidocaine and 11 adverse reactions affecting 53% (8 of 15) of patients taking tocainide occurred. Four patients in each treatment group suffered dose-limiting adverse effects. This study suggests that the efficacy and safety of intravenous tocainide are similar to that of intravenous lidocaine in patients with chronic ventricular arrhythmias.

Anti-Arrhythmia Agents↗

Cibenzoline-induced hypoglycemia.

Antiarrhythmic-induced hypoglycemia is an ill-defined phenomenon. Sporadic cases have been reported with disopyramide, a class IA antiarrhythmic agent. We report a case of cibenzoline-induced hypoglycemia in an elderly male with a history of ischemic heart disease, congestive heart failure, ventricular arrhythmias, and chronic obstructive pulmonary disease. Cibenzoline is a class I antiarrhythmic agent currently undergoing clinical investigation in the U.S. The initial hypoglycemic episode occurred after two years of successful treatment with cibenzoline. Blood glucose during the first hypoglycemic episode was 40 mg/dL. The hypoglycemia was associated with central nervous system depression, hyperkalemia, electrocardiographic abnormalities, and respiratory distress. Rechallenge with cibenzoline resulted in recurrence of symptoms and a blood glucose level of 21 mg/dL. A second rechallenge resulted in symptoms suggestive of hypoglycemia, but cibenzoline was discontinued before frank hypoglycemia and hyperkalemia recurred. Hypoglycemia occurred during periods of fasting, which most likely ruled out reactive-type hypoglycemia. Insulinoma was ruled out by the presence of normal fasting blood glucose and plasma insulin levels. It was concluded that this patient's hypoglycemia was secondary to cibenzoline. Hypoglycemia is a rare and sporadic adverse effect associated with antiarrhythmic therapy. However, the severity of these reactions warrants increased awareness of their occurrence in patients presenting with symptoms of hypoglycemia who are receiving disopyramide or cibenzoline.

Aged↗

Multiple pulmonary neurofibromas with hypoxemia. Occurrence due to pulmonary arteriovenous shunts within the tumors.

A 62-year-old woman with multiple neurofibromas of the lung was found to have severe hypoxemia due to right-to-left shunting within the tumors. Pulmonary angiograms demonstrated that the major area of shunting was in a large tumor mass in the right lower lobe. Pathologically the neurofibromas were vascular with hyperplastic small arteries and arterioles and large dilated veins. Multiple pulmonary neurofibromas are rare; and, to our knowledge, never previously reported in association with pulmonary arteriovenous shunting.

Female↗

Lidocaine-induced second-degree mobitz type II heart block.

Lidocaine-induced atrioventricular (AV) conduction disturbances are an ill-defined phenomenon. Electrophysiological studies in both animal and human subjects have shown that therapeutic doses of lidocaine have no significant effect on AV nodal and His-Purkinje conduction time in the presence of intact AV conduction. Sporadic reports of accelerated AV conduction or complete heart block following lidocaine administration have been published. One case of Mobitz type II heart block has been reported in a patient with a prolonged QTc interval (0.61 sec) who was also receiving prenylamine. Electrophysiological studies designed to evaluate lidocaine's effects on AV conduction present conflicting observations. We report a case of Mobitz type II heart block following therapeutic doses of lidocaine in the absence of acute myocardial infarction or concomitant cardioactive drug administration. This case, in conjunction with other reported data, suggests the occurrence of lidocaine-induced AV block to be unpredictable. Although its occurrence may be infrequent, the severity of these reactions warrants careful selection and monitoring of patients who are to receive lidocaine.

Aged↗

Cardiac conduction defects in patients older than 60 years with aortic stenosis with and without mitral anular calcium.

The prevalence of conduction defects was investigated in 51 patients older than 60 years with aortic stenosis (AS) who underwent aortic valve replacement. Thirty one of the 51 patients, (61%) had associated mitral anular calcium (MAC). The mean age and prevalence of coronary artery disease, systemic hypertension and diabetes mellitus were similar in both groups. The prevalence of conduction defects (atrioventricular block, sinoatrial disease, bundle branch block, left anterior hemiblock or intraventricular conduction defect) was 18 of 31 (58%) in patients with MAC and 5 of 20 (25%) in patients without MAC (p less than 0.025). We conclude that patients older than 60 years with AS have a high prevalence of MAC, and that the prevalence of conduction defects is higher in patients older than 60 years with combined AS and MAC than in patients with AS without MAC.

Age Factors↗

Correlation between calcific aortic stenosis diagnosed by two-dimensional echocardiography and cardiac catheterization.

This retrospective study correlates the severity of calcific aortic stenosis determined by two-dimensional (2-D) echocardiography with the aortic valve area determined by catheterization in 57 patients. Aortic valve leaflet calcification was diagnosed by cineangiography in 50 (88%) of 57 patients and by 2-D echo in 57 (100%) of 57 patients (p less than 0.025). An agreement between severity of aortic stenosis by catheterization and 2-D echo occurred in 22 (39%) of 57 patients. Chi-square and logistic regression analyses showed no correlation between the severity of aortic stenosis and the 2-D echo variables: left ventricular wall thickness, left ventricular diastolic dimension, left ventricular systolic dimension, aortic root diameter, and left atrial dimension. We conclude that 2-D echo detects aortic leaflet calcification better than cineangiography. However, the severity of aortic stenosis determined by 2-D echo correlates poorly with the severity of aortic stenosis determined by cardiac catheterization.

Aged↗

The value of early out-patient cardiac exercise programmes for the elderly in comparison with other selected age groups.

To evaluate potential benefits that elderly cardiac patients might gain from early exercise programs, 361 cardiac patients were studied. Seventy-six patients were older than 65 years (elderly). All patients participated in a 12 week exercise program within six weeks of myocardial infarction or cardiac surgery. All patients performed symptom limited exercise tests prior to and after completion of the exercise program. Comparison of pre- and post-training data revealed that elderly patients had significant decrease in body weight, percent body fat, resting heart rate, submaximal average double product, and submaximal average rating of perceived exertion, P less than 0.05. Maximal achieved heart rate and mets significantly increased, P less than 0.05. Comparison of magnitude of changes seen in the elderly with those of younger patients failed to reveal significant differences, P greater than 0.05. These results suggest that the benefits of early exercise program seen in younger patients may also be expected in elderly patients.

Adult↗

Clinical and echocardiographic characteristics of patients with mitral anular calcification. Comparison with age- and sex-matched control subjects.

The clinical and echocardiographic features of 104 patients (53 women and 51 men) with mitral anular calcification (MAC) were compared with those of 121 age- and sex-matched control subjects (62 women and 59 men) without MAC. The incidence of coronary artery disease, rheumatic heart disease, systemic hypertension, and diabetes mellitus was similar in both groups. Patients with MAC had a greater incidence of cardiomegaly (p less than 0.001), cardiac conduction defects (p less than 0.001), and aortic outflow tract murmurs (p less than 0.005) than did control patients. Patients with MAC and without aortic root calcification had a higher incidence (p less than 0.001) of conduction defects than did patients with aortic root calcification without MAC. Control patients with and without aortic root calcification had a similar incidence of conduction defects. A higher incidence of atrioventricular block (p less than 0.025) and bundle branch block or left anterior hemiblock or intraventricular conduction defect (p less than 0.05) was present in anterior MAC than in posterior MAC. In conclusion, patients with MAC have a higher incidence of cardiomegaly, cardiac conduction defects, and aortic outflow tract murmurs than a control group.

Age Factors↗

Serial ambulatory monitoring in patients with unstable angina pectoris.

We performed a prospective study by dual-channel ambulatory monitoring performed for 24 to 72 hours immediately after hospitalization for unstable angina. The incidence of ST-segment depression or elevation or ventricular tachycardia or complex premature ventricular complexes (PVCs) in 42 consecutive patients with unstable angina due to coronary artery disease (39 by coronary arteriography) was investigated. During ambulatory monitoring, 28 of 42 patients (67%) exhibited ST-segment depression or elevation, 13 of 42 patients (31%) had ventricular tachycardia or complex PVCs, and 31 of 42 patients (74%) had either ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ventricular tachycardia or complex PVCs occurred in 10 of 20 patients (50%) with abnormal left ventricular function and in 3 of 22 patients (14%) with normal left ventricular function (p less than 0.025). We found that 72 hours of ambulatory monitoring was not more useful than 48 hours in detecting the incidence of ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ambulatory monitoring did not help in clinically differentiating patients with left main or 3-vessel disease from 1-vessel or 2-vessel disease. In addition, ambulatory monitoring did not help in predicting which patients with unstable angina would require coronary artery surgery.

Aged↗

Tocainide kinetics in congestive heart failure.

Our subjects were 20 patients with life-threatening or symptomatic ventricular arrhythmias refractory to standard oral antiarrhythmic drugs but responsive to intravenous lidocaine. After evaluation of arrhythmias and treatment with intravenous lidocaine, oral tocainide dosage regimens were based on age, weight, and clinical status. During initial tocainide treatment, six plasma tocainide concentrations were recorded within a single dosing interval in 17 of 20 patients, by which standard kinetic parameters were calculated. Eventual trough steady-state tocainide plasma concentrations were predicted from the derived patient-specific kinetic parameters. Mean daily tocainide dose was 1800 mg (1200 to 2400). Mean daily tocainide doses (milligram per kilogram) did not differ significantly among responders and nonresponders or among patients with or without congestive heart failure. Mean peak and trough plasma concentrations 48 hr after initiation of therapy were 9.8 and 7.5 mcg/ml. Tocainide plasma concentrations did not correlate with responders and nonresponders or identify patients who were developing adverse reactions to tocainide. There were no significant differences in any of the calculated kinetic parameters as a function of response to tocainide or the presence of congestive heart failure, but there was a trend toward smaller volumes of distribution and higher average plasma concentrations at steady state in patients with congestive heart failure. There were no significant kinetic differences among patients with and without congestive heart failure, but a trend toward higher plasma concentrations in patients with congestive heart failure and the small number of patients suggests that further data collection is necessary before dosage recommendations can be made.

Adult↗

After myocardial infarction. How to determine future risk and what to do then.

Management of the postinfarction patient should be directed toward identifying and treating individuals at risk of future coronary morbidity or mortality. The history, physical examination, resting ECG, and chest film, supplemented with ambulatory electrocardiographic monitoring, noninvasive assessment of left ventricular function, graded exercise testing, and sometimes angiography allow stratification of patients into high- and low-risk subgroups. A program of exercise training, risk factor modification, and prophylactic therapy with beta blockers would be warranted in most patients. Use of antiarrhythmic agents may alter prognosis in certain subgroups. Evidence is currently insufficient to warrant routine use of anticoagulant or antiplatelet agents in the postinfarction patient.

Adrenergic beta-Antagonists↗

Malposition of a transvenous cardiac electrode associated with amaurosis fugax.

A 55-year-old male received a transvenous ventricular pacemaker for sick sinus syndrome. After pacemaker insertion, he developed recurrent episodes of amaurosis fugax. The source of thromboemboli was the pacemaker electrode malpositioned in the left ventricle. Position of the electrode was diagnosed correctly by two-dimensional echocardiography. The malpositioned electrode was successfully removed with cessation of recurrent thromboembolic phenomenon.

Blindness↗