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Biomedical subjects

A S Manolis

Publications and source records attributed to A S Manolis.

80 records · Page 5Linked to original sources
PubMed1988

Echocardiographic and clinical correlates in drug addicts with infective endocarditis. Implications of vegetation size.

Thirty-four drug addicts with endocarditis were studied to evaluate the prognostic significance of vegetation size and its short-term changes, as determined by two-dimensional echocardiography. Among 43 episodes of endocarditis, vegetations were detected in 27 (63%), confined to the tricuspid valve in 20 patients, mitral valve in one, aortic valve in two, and both tricuspid and mitral valves in four. All vegetations were large (greater than or equal to 1 cm) (mean maximal dimension, 1.7 +/- 0.5 cm). Medical cure was achieved in all 16 patients without vegetations and in 18 (90%) of 20 patients with tricuspid valve vegetations. One patient with tricuspid vegetation and polymicrobial infection died of respiratory failure. Surgery was required for one patient with tricuspid vegetation, all three patients with isolated left-sided endocarditis, and two of four patients with multivalve involvement. Short-term changes of tricuspid valve vegetations during therapy (one to eight weeks) did not correlate with clinical outcome. Although large tricuspid vegetations may occasionally identify a subset at risk for complications, most patients with isolated tricuspid valve endocarditis have a benign prognosis.

Adult↗
PubMed1987

Short-term hemodynamic effects of intravenous methyldopa in patients with congestive heart failure.

The acute hemodynamic effects of intravenous methyldopa were studied in six patients with chronic congestive heart failure (New York Heart Association class IV) at 4-6 hours after a 750-mg bolus (period A) and 6-12 hours after a maintenance infusion of 1-2 mg/minute (period B). For period A, the most consistent and striking finding was a significant (48%) fall in pulmonary wedge pressure (33 +/- 6 to 17 +/- 2 mm Hg; p less than 0.05). Stroke volume increased 39% (23 +/- 3 to 32 +/- 4 ml/m2; p less than 0.05), while peripheral vascular resistance decreased 15% (3331 +/- 363 to 2841 +/- 241 dynes.s.cm-5; p less than 0.05). Heart rate fell from 97 +/- 7 to 76 +/- 3 beats/minute (p less than 0.05) with a nonsignificant decline in mean right atrial pressure (18 +/- 4 to 9 +/- 1 mm Hg). These hemodynamic changes were either sustained or enhanced during period B. Concomitant clinical improvement was also noted. As an agent with potent vasodilatory and antiadrenergic properties, methyldopa permitted a rise in stroke volume by virtue of unloading and possible inhibition of sympathetic activity that led to increased density of beta-adrenergic receptors of the heart (up-regulation). Significant reduction of ventricular filling pressure was attributed to venodilation and probable improved diastolic function. In selected patients with severe congestive heart failure, particularly underscored by excessive sympathetic tone, methyldopa may be considered as an alternative agent to improve cardiac performance and clinical symptomatology.

Aged↗
PubMed1987

Cardiopathia fantastica and arteritis factitia as manifestations of Munchausen syndrome.

We describe three patients, each with a cardiovascular presentation of Munchausen's syndrome. Two patients' symptoms masqueraded as unstable angina (cardiopathia fantastica); one required intra-aortic balloon counterpulsation, while repeated cardiac catheterizations revealed normal coronary arteries. The third patient, with at least 27 documented hospital admissions, first presented as the cardiopathia fantastica variety and progressed to recurrent thromboembolism and limb amputations as a result of iatrogenic complications induced by angiographic and surgical procedures (arteritis factitia).

Adult↗
PubMed1987

Supraventricular tachycardia. Mechanisms and therapy.

The insights into the mechanisms of supraventricular tachycardia provided by the techniques of intracardiac recording and programmed cardiac stimulation have had a major impact on our therapeutic approach to this common problem. These techniques have led to a more systematic analysis and precise interpretation of the standard surface electrocardiogram. An accurate diagnosis of the mechanism of supraventricular tachycardia can be made in the majority of patients using the electrocardiogram aided by special leads (eg, Lewis leads) and bedside maneuvers. Identification of the likely electrophysiologic mechanism allows for a more rational and effective approach to both acute and chronic therapy.

Diagnosis, Differential↗
PubMed1987

Atypical pulmonary and neurologic complications of amiodarone in the same patient. Report of a case and review of the literature.

Atypical manifestations of pulmonary toxicity and previously unreported autonomic nervous system dysfunction complicating amiodarone therapy were observed in a patient being treated for sustained ventricular tachycardia. Pulmonary and hepatic nodules on computed tomographic scan masquerading as metastatic carcinoma were initially noted. Focal infiltrates and a large left pleural effusion mimicking infection, malignant neoplasm, or collagen vascular disease became manifest at a later stage. Autonomic dysfunction presented as incapacitating orthostatic hypotension and persisted for six weeks after amiodarone withdrawal. The pleuropulmonary toxic effects were reversible on discontinuation of amiodarone therapy, and resolution was hastened by short-course steroid treatment.

Aged↗
PubMedDate not supplied

The control of dyslipidemia in outpatient clinics in Greece (OLYMPIC) Study.

The objective of this study was to determine the proportion of Greek patients referred to outpatient clinics for dyslipidemia who achieved the low-density lipoprotein cholesterol (LDL-C) goal defined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines, using lifestyle changes, lipid-lowering drug treatment (LLDT), or both. Adult patients with dyslipidemia, who had been receiving a hypolipidemic diet and/or LLDT for at least 3 months were assessed in a multicenter study performed at 66 sites across Greece. Patients were followed up for an additional 3-month treatment period. Lipid levels were recorded at baseline and at the end of the study. The primary endpoint was the proportion of patients achieving their individual LDL-C target at the end of the study, according to their coronary heart disease (CHD) risk status or its equivalents, as defined by the NCEP-ATP III guidelines. Multivariate logistic models were used to identify determinants of undertreatment. The study included 2,660 adults (20-75 years) from 7 regions of Greece. Of the evaluable sample (n = 2,211; men 51%; mean age 62 +/-9 years) 81% were receiving LLDT (96% with statins and 3% with fibrates), 44% had a history of CHD, 61% arterial hypertension, 36% diabetes, and 26% a family history of premature CHD. Overall, 6% were at low CHD risk, 30% at medium CHD risk, and 63% at high CHD risk. At the end of the study, 26% of all patients and 30% of those receiving LLDT achieved the NCEP-specified LDL-C target levels. The percentage of patients at LDL-C goal according to CHD risk status was: low risk 67% (95% CI = 59-75), medium risk 29% (95% CI = 26-33), and high risk 20% (95% CI = 18-22). Statins proved to be more effective than fibrates (p <0.0001). Atorvastatin-treated subjects (n = 1,222, mean dose 19 mg/day) attained the LDL-C target (31% of the cases) at a higher rate than those receiving other LLDT (n = 574, 26% at target, p <0.01) or not receiving drug treatment (n = 415, 8%, p <0.001). This outcome was more evident in the high-CHD risk group (n = 1,402, 26% with atorvastatin vs 16% with other LLDT and 3% not receiving LLDT attained the LDL-C goal, ANOVA, p <0.001). The majority of dyslipidemic patients receiving LLDT, mainly those with high-CHD risk, are not achieving the NCEP LDL-C target. This is mainly explained by inadequate dose titration to ensure target goals are met. Promoting healthy lifestyle and appropriate LLDT (potent statins with sufficient dose titration) must be implemented to ensure that patients attain LDL-C treatment goals and thus benefit from the reduction in individual CHD risk.

Adult↗