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S Charlap

Publications and source records attributed to S Charlap.

At least 19 recordsLinked to original sources
PubMed1990

R- and S-wave amplitude changes with acute anterior transmural myocardial ischemia. Correlations with left ventricular filling pressures.

The value of R- and S-wave amplitude changes as electrocardiographic (ECG) markers of myocardial ischemia and dysfunction was evaluated using coronary angioplasty as a model of acute transmural ischemia and ST segment elevation. Hemodynamic data and 12-lead ECGs were recorded at baseline and during coronary occlusion in 34 patients with left anterior descending artery angioplasty. In the precordial leads V1 through V4, the sum of R-wave amplitude increased in 17 patients, was unchanged in ten, and decreased in seven; the sum of S-wave amplitude decreased in 33 patients (including two patients with complete loss of S wave) and increased in one. Mean R-wave change was 2.7 +/- 6.2 mm, mean S-wave change was -12.9 +/- 9.0 mm, and mean precordial ST elevation was 12.5 +/- 8.7 mm. Absolute R-wave change correlated directly with ST elevations (p = .013), while S-wave change correlated inversely (p less than .007). Only ST elevations correlated with changes in pulmonary capillary wedge pressure (PW) (p less than .007). In the precordial lead with maximum ST elevations, only R-wave changes correlated with ST elevations (p = .002), and both R-wave changes and ST elevations correlated with changes in PW (R:p = .027; ST:p = .007). The presence of large increases in R waves or decreases in S wave, or of high-magnitude ST elevations identified patients with the highest elevations in PW. In conclusion, decreases in S waves and, less commonly, increases in R waves are seen with diagnostic ST elevations and may have some limited clinical value. The correlation between magnitude of acute anterior ST elevations and changes in left ventricular filling pressures may have important clinical consequence.

Acute Disease↗
PubMed1989

Effects of occlusion of the left anterior descending coronary artery during angioplasty on right-sided cardiac pressures and electrocardiographic changes.

Controversy persists regarding the presence and extent of right ventricular involvement with acute anterior injury. Also unclear are the incidence and significance of ST elevations in the right-sided leads in acute left anterior descending artery occlusion. Baseline and coronary occlusion hemodynamics and 15-lead electrocardiograms (addition of RV3 through RV5) were recorded in 42 patients during 32 left anterior descending and 13 right coronary artery angioplasties. The right coronary and left anterior descending artery angioplasties had similar baseline right and left ventricular hemodynamics, as well as identical right atrial to pulmonary wedge pressure ratios (0.51 right coronary vs 0.51 left anterior descending). Whereas the right coronary and left anterior descending occlusions produced similar elevations in right ventricular filling pressures, the left anterior descending occlusions produced greater elevations in left ventricular filling pressures. The right atrial to pulmonary wedge ratio increased with right coronary occlusions, but was unchanged with left anterior descending occlusions (0.79 right vs 0.46 left, p less than or equal to 0.0001). Presence of right-lead ST elevations in 10 left anterior descending occlusions did not con-note increased right ventricular filling pressures, but did suggest increased left ventricular ischemia and dysfunction. In conclusion, right ventricular dysfunction, as manifested by increased filling pressures, is seen with both right coronary and left anterior descending occlusions. Although it is the predominant abnormality in right coronary occlusions, in left anterior descending occlusions it is proportional to left ventricular dysfunction. ST elevations in a right lead with left anterior descending occlusions do not constitute a marker for increased right ventricular dysfunction.

Angioplasty, Balloon↗
PubMed1989

Pericardial effusion early in acute myocardial infarction.

The incidence and significance of pericardial effusions early in acute myocardial infarction remain unclear. Using two-dimensional echocardiography, 172 patients with an acute myocardial infarction were evaluated within 72 h of presentation. Thirty patients (17%) had a pericardial effusion (29 small, 1 moderate) while 142 (83%) did not. No patient developed cardiac tamponade or required pericardiocentesis. Patients with pericardial effusions had higher peak creatine kinase as compared to patients without effusions (2036 +/- 1466 vs. 1483 +/- 1241, p less than 0.05) and a greater number of aneurysms (20% vs. 6%, p less than 0.05). In-hospital mortality was higher in the patients with pericardial effusions (10% vs. 2%, p less than 0.05). In conclusion, pericardial effusions are common in the early AMI period but are generally small and hemodynamically insignificant. They are associated with larger infarcts and greater mortality.

Aged↗
PubMed1989

Labetalol compared with propranolol in patients with both angina pectoris and systemic hypertension: a double-blind study.

Labetalol is a non-selective beta-adrenoceptor antagonist agent with added alpha 1-adrenergic blocking properties, beta 2-stimulating action, and direct vasodilatory activity. A multi-center, double-blind, parallel group study compared the safety and efficacy of labetalol to propranolol in the treatment of patients with both exertional angina and mild to moderate systemic hypertension. An initial 4 to 5 week placebo washout phase was followed by a five week titration phase and a four month maintenance phase. Labetalol and propranolol had similar effects in reducing supine and standing blood pressures, except for a greater reduction in standing systolic blood pressure seen in the labetalol group. There were comparable effects by both treatments on angina attacks, nitroglycerin use, and exercise tolerance. Adverse effects were frequent with both drugs, but were generally minor. Thus, labetalol appears to be an effective alternative to propranolol in the treatment of patients with coexisting angina pectoris and hypertension, with the choice of agent dependent on the clinical situation.

Adult↗
PubMed1989

Anticipation of bypass surgery: can it induce silent myocardial ischemia?

Psychological stress has been demonstrated to induce myocardial ischemia. To determine whether stressful events before a coronary artery bypass grafting procedure precipitate myocardial ischemia, silent or symptomatic, and whether this can have an effect on the prognosis, 26 patients were evaluated before a bypass operation with continuous Holter monitor recording. Specific events monitored were signing surgical consent, receiving preoperative medications, shaving and preparing, and transfer to the operating room. A positive Holter result was defined as an ST segment depression of 1 mm or more lasting one minute or longer. Six patients (23%) were found to have one or more episodes of substantial ST segment depression, with a total of ten episodes lasting 208 minutes recorded. All episodes were silent and not associated with an increase in mean heart rate. The majority of episodes occurred randomly, although three episodes did occur between 5 and 6 AM at the time of transport to the operating room. This appeared to be related more to the circadian rhythm than to the stress of transport. No perioperative or postoperative myocardial infarctions occurred, and all patients were alive at 30 days. In conclusion, silent myocardial ischemia present in the immediate preoperative period does not appear to be related to specific preoperative events. Frequency of early morning ischemia may warrant changes in the medication schedule to provide additional protection during these hours.

Aged↗
PubMed1989

Angiotensin-converting enzyme inhibitors in heart failure.

Recognition of the importance of the renin-angiotension-aldosterone system in heart failure, along with an appreciation of the hemodynamic benefits of vasodilator therapy has led to the widespread use of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure. The ACE inhibitors are the only class of vasodilator agents shown to have a significant protective effect against mortality in patients with heart failure.

Aldosterone↗
PubMed1989

Calcium antagonists and heart failure.

The systemic vasodilatory actions of the calcium antagonists make them potentially attractive for use as afterload reducing agents in patients with left ventricular failure. However, unlike other vasodilator drugs, these drugs also exert a direct negative inotropic effect on the myocardium. Clinical data suggest a limited role for the calcium antagonists as vasodilator therapy in patients with heart failure.

Calcium Channel Blockers↗
PubMed1989

Nitrates in congestive heart failure.

An important role for nitrates in the treatment of patients with congestive heart failure has been demonstrated. By dilating the venous and arterial vasculature, they improve hemodynamics as well as exercise tolerance. Attenuation of nitrate action that occurs with chronic therapy can be minimized by following certain treatment strategies.

Heart Failure↗
PubMed1989

Beta-adrenergic blocking drugs in the treatment of congestive heart failure.

Experimental and clinical data suggests that increased serum catecholamines may have predominantly detrimental effects in patients with congestive heart failure. Some investigators have proposed use of beta-blockers in heart failure as a means of ameliorating the harmful effects of the excess catecholamines. The clinical experience to date with use of these agents as therapy in congestive heart failure is limited but does suggest a future role for beta-blockers as adjunct therapy in a select population of patients with heart failure.

Adrenergic beta-Antagonists↗
PubMed1988

Serotonergic blockade compared with beta-adrenergic blockade in systemic hypertension: a double-blind comparison of ketanserin with propranolol.

The safety and efficacy of ketanserin, a competitive serotonin blocking agent, and propranolol were compared in 33 patients with mild to moderate hypertension (sitting diastolic blood pressure [DBP] 95-115 mm Hg) using a placebo run-in, randomized, double-blind parallel study design. All patients received placebo for 4 weeks, then were randomized to receive increasing doses of either ketanserin (20, 40 mg twice daily) or propranolol (40, 80 mg twice daily) to achieve a goal sitting DBP less than 90 mm Hg. Patients not achieving the goal blood pressure with either drug as monotherapy, received the other drug in combination. At the end of the active monotherapy phase (week 10 of the study), propranolol demonstrated a greater decrease in DBP from baseline, as compared to ketanserin (-7.9 +/- 10.9 mm Hg with propranolol, P less than 0.05; -1.0 +/- 7.2 mm Hg with ketanserin, P = NS). Four out of 16 patients achieved goal response on propranolol, compared to 3/17 for ketanserin. With combination treatment, 9/18 patients reached the goal response; the addition of propranolol to ketanserin in non-responders resulted in further reduction of sitting DBP of -10.3 +/- 6.3 compared to monotherapy (P less than 0.001), while the addition of ketanserin to non-responders produced no significant response in sitting DBP. Propranolol showed a consistent effect in slowing heart rate. Ketanserin displayed less frequent side effects than propranolol. Propranolol used twice daily appears to be more effective than twice daily ketanserin use in patients with mild to moderate hypertension.

Adrenergic beta-Antagonists↗
PubMed1988

Alpha-adrenergic blockers.

alpha-Adrenergic blockers are important drugs in the treatment of hypertension and other cardiovascular and noncardiovascular disorders. The ability to selectively block alpha-receptor subtypes provides a greater margin of safety and efficacy for these drugs.

Adrenergic alpha-Antagonists↗
PubMed1988

Diltiazem, nifedipine, and their combination in patients with stable angina pectoris: effects on angina, exercise tolerance, and the ambulatory electrocardiographic ST segment.

The efficacy and safety of oral nifedipine and diltiazem were compared in 20 patients with stable angina pectoris with use of a placebo run-in, randomized, double-blind titration to maximal effect crossover protocol. The effects of treatment withdrawal were also analyzed. All patients received placebo for 2 weeks and were then randomly assigned to receive either diltiazem or nifedipine. A 2 week drug titration phase in which patients received either diltiazem (180 to 360 mg/day) or nifedipine (30 to 120 mg/day) in three divided doses was followed by a 1 week maintenance phase. Patients then received placebo for 1 to 2 weeks, followed by crossover to the other treatment regimen and a second placebo washout period of 1 week. Patients (n = 13) who remained symptomatic on both diltiazem and nifedipine during the monotherapy periods entered a 3 week combination treatment phase, followed by a final 1 week placebo washout period. Frequency of angina, nitroglycerin consumption, exercise tolerance (Naughton protocol), and frequency of daily episodes of ST segment deviations on the electrocardiogram (1 mm of ST segment depression persisting for at least 1 min with and without chest pain) on an ambulatory electrocardiographic monitor were assessed during the baseline placebo, active monotherapy, placebo withdrawal, and combination treatment phases. Plasma drug levels were also measured. Compared with initial placebo values, the frequency of angina and the amount of nitroglycerin treatment were reduced by both diltiazem (p less than .001) and nifedipine (p less than .02). Diltiazem was more effective than nifedipine in reducing angina (p less than .02). Exercise duration increased with both drugs (p less than .0001). Diltiazem was significantly better than nifedipine in reducing the episodes of ST segment depression on the ambulatory monitor (p less than .01). Diltiazem reduced the resting heart rate (p less than .01); both drugs reduced the resting blood pressure and rate-pressure product. Overall, combination therapy was more effective in patients who did not maximally respond to diltiazem or nifedipine alone with respect to anginal and exercise variables and in reducing blood pressure at rest and during exercise. Plasma drug levels could not predict an individual patient's treatment response. Diltiazem may increase nifedipine drug levels when the drugs are combined. Fewer side effects were observed with diltiazem than nifedipine; the most side effects were seen with combination treatment. There were no apparent withdrawal effects observed with either treatment regimen.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗
PubMed1987

Enalapril: a long-acting angiotensin-converting enzyme inhibitor.

The development of angiotensin-converting enzyme (ACE) inhibitors is of landmark importance in the understanding and treatment of cardiovascular disorders, particularly hypertension and congestive heart failure. Enalapril has recently joined captopril as an approved, orally active ACE inhibitor. Like captopril, it has been effective in the treatment of hypertension and congestive heart failure, with minimal adverse reactions noted. Differences in pharmacology exist between enalapril and captopril which may prove to be of clinical significance.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Long-term safety and efficacy comparison of immediate-release and sustained-release oral verapamil in systemic hypertension.

The long-term safety and efficacy of twice-daily sustained-release verapamil were assessed compared to thrice-daily immediate-release verapamil in 25 patients with mild to moderate systemic hypertension. Patients were monitored on immediate-release verapamil (480 mg/day) for 6 months and were then placed on twice-daily sustained-release verapamil for an additional 6 months. Immediate-release verapamil, with and without a diuretic, successfully controlled standing and sitting systolic and diastolic blood pressures (p less than 0.001) compared to pretreatment baseline values. The effects of verapamil on blood pressure were sustained for an additional 6 months when the sustained-release formulation was utilized. Both formulations were well tolerated, with no significant effects on heart rate. In conclusion, verapamil, in both the immediate- and sustained-release formulations, is equally effective in lowering blood pressure for up to 1 year.

Administration, Oral↗
PubMed1987

Calcium-channel blockers for combined systemic hypertension and myocardial ischemia.

Scientific rationale suggests a potentially important role for the calcium-channel blockers in the treatment of patients with coexisting systemic hypertension and coronary artery disease. Clinical investigation confirms the usefulness of these drugs as monotherapy in the treatment of patients with chronic stable angina and mild-to-moderate hypertension. There are several therapeutic effects of the calcium-channel blockers in coronary artery disease. Beneficial actions on the major determinants of oxygen consumption, i.e., heart rate, blood pressure, and contractility, are generally seen. The potent coronary vasodilating actions of these drugs allow for increased coronary blood flow and alleviation of coronary vasospasm. The effectiveness of the calcium-channel blockers in hypertension appears to be primarily due to their ability to induce systemic vasodilation. Improvements in ventricular compliance, regression of left ventricular hypertrophy, and cardioprotection appear to be additional beneficial effects of the drugs. Calcium-channel blockers compare favorably with beta-blockers; they appear to be more effective than some beta-blockers in the treatment of hypertension in the elderly and black population and can be given to patients with bronchospasm or peripheral vascular disease. Calcium-channel blockers are a welcome addition to existing drug regimens available for the management of patients with concomitant coronary artery disease and systemic hypertension.

Angina Pectoris↗
PubMed1986

Calcium-channel blockers for combined angina pectoris and systemic hypertension.

Calcium-channel blockers have been successfully used in the treatment of angina of effort and systemic hypertension. Many patients present with concomitant angina pectoris and hypertension. Controlled clinical trials demonstrate that the calcium-channel blockers are safe and effective as monotherapy in the treatment of these patients, and that their use compares favorably with that of propranolol. The effectiveness of these agents in hypertension appears to be primarily due to their ability to induce systemic vasodilation. Calcium-channel blockers have several therapeutic effects in angina pectoris. Beneficial actions on the major determinants of oxygen consumption, i.e. heart rate, blood pressure and contractility, are generally seen. The potent coronary vasodilating actions of these agents allow for increased coronary blood flow. Improvements in ventricular compliance, regression of left ventricular hypertrophy and cardioprotection appear to be additional effects of the calcium-channel blockers; their contribution to the drugs' overall therapeutic efficacy is presently being evaluated. Calcium-channel blockers are a welcome addition to drug regimens available for the management of patients with coexisting angina pectoris and hypertension.

Adult↗