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Biomedical subjects

P F Cohn

Publications and source records attributed to P F Cohn.

At least 73 records · Page 4Linked to original sources
PubMed1986

Total ischemic burden: definition, mechanisms, and therapeutic implications.

The concept of the total ischemic burden includes all types of ischemia encompassing both silent and symptomatic ischemic episodes. This concept is currently causing a re-evaluation of current therapeutic goals for patients with coronary heart disease. Although the mechanism of cardiac pain is still unclear, we do have some information about other pathophysiologic mechanisms at work in this disorder. We think of ischemia as occurring secondary to reduced supply (primary ischemia), increased demand (secondary ischemia), or a combination of the two (mixed ischemia). Because of the lower heart rate associated with many episodes of ischemia during everyday activities, suggesting that vasoconstriction is playing a role in the patient's supply/demand imbalance, calcium antagonists appear to be particularly useful agents for the treatment of vasoconstriction in patients with angina.

Adrenergic beta-Antagonists↗
PubMed1986

Prognostic significance of asymptomatic coronary artery disease.

Prognosis in the various forms of asymptomatic coronary artery disease is not precisely defined but available data suggest that it may not be as benign as previously thought. This is especially true in patients with silent myocardial ischemia, 3-vessel disease and poor exercise tolerance, because many of these patients may go on to sudden death or myocardial infarction. It is also true in patients with silent myocardial infarctions, because prognosis in this type of myocardial infarction is similar to that of patients with symptomatic infarctions.

Adult↗
PubMed1986

A new use for M-mode echocardiography in detecting left ventricular diastolic dysfunction in coronary artery disease.

Regional left ventricular (LV) diastolic function affects the global rate and pattern of LV filling. These changes may be detected by changes in the magnitude and timing of the increase in LV basal diameter during diastole. Because M-mode echocardiography possesses the high temporal and spatial resolution to detect such abnormalities, a group of 8 normal control subjects were compared with a group of 12 patients with coronary artery disease (CAD) to determine differences in the rate and timing of ventricular filling. The CAD patients had lower rates of fast filling expansion than the control subjects. The proportion of LV diastolic expansion during fast filling was lower. During atrial systole the increased rate of LV expansion was not significantly higher in the CAD patients, but the proportion of diastolic expansion occurring with atrial systole was increased. These changes may reflect a decrease in the rate and magnitude of early diastolic filling in the noncompliant ventricle and an increased reliance on active atrial transport. Thus, CAD alters the rate and pattern of LV filling. Changes in LV diameter as measured by M-mode echocardiography may be useful in detecting altered patterns of LV diastolic filling and identifying patients with CAD.

Adult↗
PubMed1986

Silent myocardial ischemia: dimensions of the problem in patients with and without angina.

Because of its possible relation to sudden cardiac death, silent myocardial ischemia is an important public health issue, especially with regard to persons who are totally asymptomatic. However, this syndrome is not confined to individuals without prior histories of angina or myocardial infarction; it is also being reported with increasing frequency in patients with clinical evidence of coronary artery disease. Although prognostic studies of silent myocardial ischemia in patients with angina are currently in progress, it appears that patients with extensive disease and left ventricular dysfunction are at highest risk for subsequent cardiac events.

Angina Pectoris↗
PubMed1986

Effect of beta blockade on silent regional left ventricular wall motion abnormalities.

The effect of beta-adrenergic blockade on regional left ventricular wall motion abnormalities was studied in 11 patients with coronary artery disease and silent myocardial ischemia during exercise testing. Four patients were asymptomatic; 7 were asymptomatic after a myocardial infarction. Left ventricular wall motion abnormalities were characterized by reduced regional ejection fraction (EF) during exercise determined by gated left anterior oblique images of the cardiac blood pool. In the 11 patients, 10 anteroseptal and 8 inferoposterior regions were subserved by stenotic coronary arteries. Before beta blockade, regional EF decreased in 15 of 18 regions. After beta blockade, this occurred in only 6 of 18 regions (p less than 0.05); the other 12 regions showed no change or an actual increase in regional EF. Thus, beta-adrenergic blockade effectively improved the reduction in exercise regional EF usually seen in patients with coronary artery disease with silent myocardial ischemia. One probable mechanism of action is a reduction in myocardial oxygen requirement at peak exercise.

Adrenergic beta-Antagonists↗
PubMed1986

Frequent episodes of silent myocardial ischemia after apparently uncomplicated myocardial infarction.

Frequent episodes of silent myocardial ischemia were documented in two patients, one with recognized and one with unrecognized prior myocardial infarction. Neither patient had symptoms after the infarction, but both demonstrated silent myocardial ischemia on exercise testing, which prompted further study with 48 hour ambulatory electrocardiographic (Holter) recordings. In each patient, heart rate recorded with the Holter monitor during the ischemic episodes was usually less than that observed during ischemia precipitated by exercise testing. This suggests that increased vasoconstrictive tone may play a role in silent ischemic episodes occurring during daily activities.

Coronary Disease↗
PubMed1986

Possible mechanisms responsible for silent myocardial ischemia: do patients with silent myocardial ischemia have altered pain thresholds?

There is some evidence that alterations in pain perception are present in patients with coronary artery disease and painless myocardial ischemia, but whether endorphins are implicated is still unclear. Further studies are also needed to document the validity of various theories of the cardiac pain mechanism itself, especially the existence of specific nociceptive sympathetic fibers.

Coronary Disease↗
PubMed1986

Myocardial ischemia without pain: recognition and clinical picture.

Recognition of the various syndromes of asymptomatic coronary artery disease often depends on the fortuitous observation of ECG abnormalities during stress testing or routine examinations. The clinical picture of silent myocardial ischemia--the most prevalent of the syndromes--depends on whether patients are totally asymptomatic, are asymptomatic after an infarction, or have angina. As with symptomatic disease, prognosis appears related to the extent of vessel disease and left ventricular dysfunction.

Coronary Disease↗
PubMed1986

Regional ejection fraction during exercise: a quantitative measurement to localize coronary artery stenoses in patients with symptomatic or silent myocardial ischemia.

To determine the ability of quantitative radionuclide ventriculography to localize coronary artery stenoses in patients with angina and silent myocardial ischemia, the authors studied changes in regional ejection fractions produced by supine bicycle exercise in 49 patients, 16 of whom had silent myocardial ischemia. For example, in 35 patients with 70 per cent or greater stenoses of the left anterior descending and/or left main coronary artery, anteroseptal regional ejection fraction fell from 55 +/- 3 per cent at rest to 50 +/- 4 per cent with exercise (p less than 0.05). In 14 patients with lesser or no stenoses of the left anterior descending and/or left main coronary artery, anteroseptal regional ejection fraction increased from 62 +/- 4 per cent at rest to 67 +/- 5 per cent during exercise (p less than 0.05). Similar findings were obtained in patients with 70 per cent or greater stenoses of the left circumflex and/or right coronary artery in whom inferoposterior regional ejection fraction was measured and compared with that in patients with lesser or no stenoses in these vessels. Thus, evaluation of regional ejection fraction allowed the localization of coronary artery stenoses in coronary patients whether or not their ischemia was accompanied by pain.

Adult↗
PubMed1985

Silent myocardial ischemia: classification, prevalence, and prognosis.

In the United States there may be four to five million patients with silent myocardial ischemia, including approximately 50,000 asymptomatic patients who have had myocardial infarction, one to two million asymptomatic patients with no history of myocardial infarction or angina, and three million patients with angina. The prognosis for patients who have had infarction and for patients with angina varies, but, in general, it is worse for patients with more extensive disease because sudden cardiac death may be the only clinical sign in asymptomatic patients. Silent myocardial ischemia is an important public health issue; it is hoped that its detection may prevent many episodes of sudden cardiac death annually.

Angina Pectoris↗
PubMed1985

Silent myocardial ischemia as a manifestation of asymptomatic coronary artery disease: what is appropriate therapy?

Silent myocardial ischemia is one of the most important clinical manifestations of asymptomatic coronary artery disease, along with silent myocardial infarction. It may well be a forerunner of sudden cardiac death. Although our understanding of the pathophysiologic mechanisms of the syndrome is still unresolved, we do know that prognosis in certain subsets of patients is far from benign. For that reason, aggressive therapy is recommended in asymptomatic patients with advanced disease, especially if they have already experienced a myocardial infarction, silent or otherwise.

Adrenergic beta-Antagonists↗
PubMed1985

Nitrate therapy in angina and congestive heart failure.

Nitrates are vasodilators of venous and arterial smooth muscle commonly prescribed both for angina and congestive heart failure. Primarily venodilators, nitrates also affect the systemic circulation if administered in sufficient dosage. In the coronary circulation, the principal effect is on the large epicardial and collateral vessels. Blood is shunted toward the ischemic subendocardium. In the majority of patients with angina, relief of symptoms by nitrates is primarily due to hemodynamic effects on preload and afterload, unless the patient has coronary spasm. In patients with congestive heart failure, nitrates decrease the resistance to the emptying of blood from the left ventricle as well as the filling pressure. Nitrates are relatively well tolerated, except for an initial throbbing headache which rapidly resolves as tolerance develops. Nitrates are available in a multitude of forms including sublingual, oral, topical, transmucosal, intravenous, and spray preparations. Oral preparations undergo a first-pass effect in the liver, requiring larger doses. Other forms avoid this problem by direct transdermal absorption or the intravenous route. The latter has the advantage of rapid administration and ease of titration. The choice of nitrate depends upon the clinical situation.

Angina Pectoris↗
PubMed1984

Comparison of lorcainide and quinidine in the treatment of ventricular ectopy.

Lorcainide, a new type I antiarrhythmic agent, was compared to quinidine in respect to antiarrhythmic efficacy and clinical safety. Thirteen subjects completed an open, randomized, crossover study with analysis of 24-hour ambulatory ECG monitoring and drug blood levels. The QRS and Q-T intervals increased with both lorcainide and quinidine. The mean reduction in total ventricular premature beats (VPBs) with quinidine was 16 percent compared to 68 percent with lorcainide (p less than .05). With lorcainide eight of 13 subjects had a significant (greater than 82 percent) reduction in VPBs compared to only three of 13 subjects taking quinidine (p less than .05). This same relationship was observed when mean VPB/1,000 heartbeats was analyzed. Ventricular tachycardia was no longer present in five of nine subjects taking lorcainide and in two of nine taking quinidine. No relationship could be established between drug level and arrhythmia suppression in this small population. Some CNS effects were reported in both groups, but no significant hematologic, chemical, or urinary adverse effects were seen with either drug. Thus, lorcainide compares favorably to quinidine in regard to arrhythmia suppression, but was limited in its clinical utility by CNS side effects.

Adult↗