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Biomedical subjects

A F Parisi

Publications and source records attributed to A F Parisi.

At least 19 recordsLinked to original sources
PubMed1992

A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. Veterans Affairs ACME Investigators.

BACKGROUND: Despite the widespread use of percutaneous transluminal coronary angioplasty (PTCA), only a few prospective trials have assessed its efficacy. We compared the effects of PTCA with those of medical therapy on angina and exercise tolerance in patients with stable single-vessel coronary artery disease. METHODS: Patients with 70 to 99 percent stenosis of one epicardial coronary artery and with exercise-induced myocardial ischemia were randomly assigned either to undergo PTCA or to receive medical therapy and were evaluated monthly. The patients assigned to PTCA were urged to have repeat angioplasty if their symptoms suggested restenosis. After six months, all the patients had repeat exercise testing and coronary angiography. RESULTS: A total of 107 patients were randomly assigned to medical therapy and 105 to PTCA. PTCA was clinically successful in 80 of the 100 patients who actually had the procedure, with an initial reduction in mean percent stenosis from 76 to 36 percent. Two patients in the PTCA group required emergency coronary-artery bypass surgery. By six months after the procedure, 16 patients had had repeat PTCA. Myocardial infarction occurred in five patients assigned to PTCA and in three patients assigned to medical therapy. At six months 64 percent of the patients in the PTCA group (61 of 96) were free of angina, as compared with 46 percent of the medically treated patients (47 of 102; P less than 0.01). The patients in the PTCA group were able to increase their total duration of exercise more than the medical patients (2.1 vs. 0.5 minutes, P less than 0.0001) and were able to exercise longer without angina on treadmill testing (P less than 0.01). CONCLUSIONS: For patients with single-vessel coronary artery disease, PTCA offers earlier and more complete relief of angina than medical therapy and is associated with better performance on the exercise test. However, PTCA initially costs more than medical treatment and is associated with a higher frequency of complications.

Adrenergic beta-Antagonists↗
PubMed1992

The value and promise of echocardiography in acute myocardial infarction and coronary artery disease.

Two-dimensional and Doppler echocardiography have become extremely useful in the management of patients with acute myocardial infarction (AMI). Echocardiography is noninvasive, relatively inexpensive, and has no known biohazards. It offers unequaled information about cardiac anatomy and function. In the acute setting it is useful in the diagnosis of AMI and its complications. It is an excellent tool for monitoring therapy. Echocardiography has been shown to be useful in risk stratification upon presentation to the emergency ward and prior to hospital discharge. Stress echocardiography has broadened and sharpened the diagnostic and prognostic information. Contrast echocardiography has promise for demonstrating coronary artery flow. Research in ultrasonic myocardial tissue characterization shows potential for differentiating ischemic myocardium from infarcted myocardium. Thus, echocardiography is likely to become increasingly important in the future management of patients with AMI.

Coronary Circulation↗
PubMed1991

Coronary bypass surgery improves survival in high-risk unstable angina. Results of a Veterans Administration Cooperative study with an 8-year follow-up. Veterans Administration Unstable Angina Cooperative Study Group.

To identify high-risk subgroups, 468 patients with unstable angina were prospectively stratified according to the clinical presentation of unstable angina (type I or type II) and left ventricular function (normal or abnormal) and were randomized to conventional medical therapy or surgical treatment with coronary bypass surgery. Type I patients (n = 374) were those who had progressive effort angina or recent angina at rest. Type II patients (n = 94) were those who had severe rest angina associated with ST-T changes on the electrocardiogram. Follow-up for 8 years showed that the cumulative mortality rates for type II patients with abnormal left ventricular function were significantly lower in the surgical patients compared with the medical cohorts (13% versus 46%, p less than 0.04). In the other subgroups, cumulative medical and surgical mortality rates were not different. Thus, type II patients with abnormal left ventricular function appear to be the subgroup of patients who are at the highest risk with medical therapy. Coronary bypass surgery significantly reduces the mortality in this high-risk subgroup of patients with unstable angina.

Angina, Unstable↗
PubMed1990

Simplified method for estimating true aortic valve mean gradient from simultaneous left ventricular and peripheral arterial pressure recordings.

Estimation of the aortic valve gradient by simultaneous recording of left ventricular and peripheral arterial pressures is subject to error due to delay and modulation of the arterial pressure contour as it propagates from the ascending aorta. This error can be corrected by averaging the mean gradients derived from unaltered and temporally aligned simultaneous left ventricular-peripheral arterial pressure tracings. In 26 patients with aortic stenosis and simultaneous recordings of ascending aortic and femoral arterial pressure we compared this method with a simplified approach in which the peripheral arterial pressure is partially aligned by advancing it against the left ventricular pressure by 50% of the time delay of the simultaneously recorded upstrokes. Gradients measured this way predicted the true aortic valve gradients (left ventricular-ascending aortic) with a mean difference of +1.1 mm Hg (range = +10 to -5 mm Hg). We recommend use of this simplified method of correction because it predicts true aortic valve gradient equally well as the averaging technique (r = 0.977 vs. 0.979) and requires half the time and effort.

Aortic Valve↗
PubMed1990

Perioperative myocardial infarction after coronary artery bypass surgery. Clinical significance and approach to risk stratification.

The clinical significance of perioperative myocardial infarction (MI) after coronary artery bypass surgery is not known. Therefore, strategies for the risk stratification of these patients do not exist. This study was undertaken to define the effect of perioperative MI on prognosis after discharge from the hospital and to develop an approach to the risk stratification of these patients. Fifty-nine patients with and 115 patients without perioperative MI were observed for 30 months for the development of cardiac events (death, nonfatal MI, and admission to hospital for unstable angina or congestive heart failure). Patients with perioperative MI were significantly more likely than patients without to have a cardiac event (31% versus 12%, p less than 0.01) and multiple events (19% versus 1%, p less than 0.001). Cox regression analysis identified two independent predictors of cardiac events other than perioperative MI (relative risk, 2.7): inadequate revascularization (relative risk, 3.5) and depressed (less than 40%) postoperative ejection fraction (EF) (relative risk, 2.1). Event-free survival rate of patients with perioperative MI varied markedly depending on the number of other negative prognostic variables present. Patients with perioperative MI who were adequately revascularized and had a postoperative EF greater than 40% had an event-free survival rate similar to patients without a perioperative MI (92% versus 87%, p = NS). Patients with perioperative MI who were inadequately revascularized and had depressed postoperative EF had an event-free survival rate of 13% (p less than 0.001 versus all other subsets). Event-free survival rate was intermediate (68%) in patients with perioperative MI and with only one of the other two variables (p less than 0.001 versus other subsets). In conclusion, perioperative MI adversely affects prognosis. Patients can be stratified into low, high, and intermediate risk subsets based on a simple assessment of the adequacy of revascularization and a determination of residual left ventricular function.

Coronary Artery Bypass↗
PubMed1989

Effects of left ventricular shape and captopril therapy on exercise capacity after anterior wall acute myocardial infarction.

The importance of left ventricular (LV) shape in determining exercise capacity was assessed in 40 male patients with LV dysfunction after anterior acute myocardial infarction (AMI). Because captopril therapy is known to improve exercise capacity in this patient population, the potential interaction between LV shape and captopril therapy was also evaluated. Patients underwent cardiac catheterization 2 to 4 weeks after AMI followed by randomization to receive placebo or captopril. LV shape was defined from biplane ventriculography by a sphericity index (volume observed/volume of sphere using long axis as diameter). Quarterly clinical assessments and maximal exercise testing were performed. A cumulative heart failure score, specific activity scale and average exercise time for the year were calculated. A greater shape distortion (increasing sphericity index) was associated with increased LV volumes, decreased ejection fraction and a larger abnormally contracting segment. Sphericity index was the only independent predictor of average exercise duration in the placebo group. Placebo-treated patients in the tercile with the most spherical ventricles had not only the lowest exercise capacity (p less than 0.01), but also accumulated the highest heart failure (p less than 0.05) and specific activity scale (p less than 0.05) scores. Captopril-treated patients with the same baseline distortion of LV shape did not manifest these shape-dependent objective and subjective measures of reduced functional capacity.

Adult↗
PubMed1989

Medical compared with surgical management of unstable angina. 5-year mortality and morbidity in the Veterans Administration Study.

We evaluated medical in comparison to surgical plus medical (surgical) treatment of unstable angina using a prospective randomized protocol that stratified patients by clinical presentation and by invasive evaluation of left ventricular (LV) function. Clinical presentations were as follows--type 1: progressive or new onset angina relieved by medication; type 2: prolonged bouts of angina poorly or incompletely relieved by medication. Abnormal LV function was arbitrarily defined as ejection fraction less than 0.50 or LV end-diastolic pressure 16 mm Hg or more. Of 468 patients, 237 were assigned to medical and 231 to surgical therapy. There were 374 type 1 and 94 type 2 patients. LV function was normal in 334 and abnormal in 134 patients. Compared with results at 24 months, this 60-month follow-up study showed important differences in survival for patients with three-vessel disease: 75% for medical and 89% for surgical patients (p less than 0.02). The cumulative 5-year rate of repeat hospitalizations for cardiac reasons was less with surgical patients for either clinical presentation. For type 1, medical patients had a 56% rate, and surgical patients had a 42% rate (p = 0.004). For type 2, medical patients had a 62% rate, and surgical patients had a 43% rate (p = 0.05). Overall mortality did not differ between the two treatments, and this remained true in type 1 versus type 2 patients and in those with normal versus abnormal LV function. However, regression analysis of medical and surgical groups with ejection fraction as a continuous variable showed that mortality of medical patients depended on ejection fraction (p = 0.004), whereas the mortality of surgical patients did not (p = 0.76), and survival in the surgical group was higher in the lowest ejection fraction tercile-73% for medical and 86% for surgical patients, p = 0.03. We conclude that surgery improves survival in patients with three-vessel disease and leads to fewer subsequent hospitalizations for cardiac reasons. An impaired ejection fraction had an adverse impact on survival of medical patients but not on surgical patients, and mortality in surgical patients was improved compared with medical patients in the lowest ejection fraction tercile.

Angina Pectoris↗
PubMed1988

Combined use of calcium-channel and beta-adrenergic blockers for the treatment of chronic stable angina. Rationale, efficacy, and adverse effects.

During the past decade, the therapy for stable angina pectoris has greatly expanded with the introduction of the calcium-channel blockers. Initially studied as monotherapy, these agents have been regularly used in combination with other antianginal medications, most notably the beta-adrenergic blockers. Although there are pharmacologic rationales for combining these agents, in daily practice, the major impetus for combination therapy is continuing angina during monotherapy. At least one well-conducted double-blind study was done to confirm that diltiazem, verapamil, and nifedipine each can markedly improve both subjective and objective measures of efficacy when used in combination with a beta-blocker. However, individual patient responses are of chief importance. Many persons do better with monotherapy than with combination treatment. The offsetting hemodynamic effects of nifedipine and a beta-blocker generally work well together; however, minor side effects are not infrequent. In the patient with underlying conduction system disease, this combination is clearly preferable. Diltiazem with a beta-blocker is usually well-tolerated, with a low incidence of adverse effects, similar to the experience with diltiazem monotherapy. Verapamil in conjunction with a beta-blocker warrants the greatest concern; approximately 10% to 15% of patients will have significant bradycardia, heart block, hypotension, or congestive failure. When these agents are used concurrently, reduced dosages, especially of the beta-blocker, will likely result in a lower incidence of adverse effects with maintained efficacy.

Adrenergic beta-Antagonists↗
PubMed1988

Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction.

We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [+/- SEM] of 21 +/- 8 ml (P less than 0.02) in the placebo group, but by only 10 +/- 6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P less than 0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P less than 0.05). Patients given captopril also had increased exercise capacity (P less than 0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.

Captopril↗
PubMed1988

The efficacy of the addition of nifedipine in patients with mixed angina compared to patients with classic exertional angina: a multicenter, randomized, double-blind, placebo-controlled clinical trial.

Episodes of myocardial ischemia in patients with coronary artery disease may be due to transient increases in coronary vasomotor tone superimposed on a fixed atherosclerotic obstruction. The purpose of this study was to determine whether identification of the clinical pattern of angina could predict the therapeutic response to the addition of nifedipine to a regimen of beta blockers and/or long-acting nitrates. Seventy-two patients with stable exertional angina were divided into two groups: "classic exertional angina" (17 patients), defined as exertional angina with a stable threshold; and "mixed angina" (55 patients), defined as exertional angina provoked by a variable threshold and/or at least two episodes of rest angina within the 3 months prior to screening. Patients were studied with nifedipine and placebo in a 6-week, double-blind, crossover design that used serial anginal diaries, exercise treadmill tests, and 24-hour ambulatory ECG monitoring. In patients with mixed angina, nifedipine reduced the frequency of angina compared to that during placebo treatment (13.1 vs 9.9 episodes/3 weeks, p less than 0.01) and reduced nitroglycerin consumption (11.7 vs 7.5 tablets/3 weeks, p less than 0.05); while in patients with classic exertional angina, nifedipine had no symptomatic effect (7.9 vs 6.8 anginal episodes/3 weeks, NS; 6.4 vs 5.8 nitroglycerin tablets/3 weeks, NS). Patients in both groups experienced a significant decrease in the manifestations of ischemia during exercise testing. Patients with mixed angina experienced a reduction in the daily frequency of painful episodes of ST segment depression during nifedipine treatment compared to placebo (0.6 vs 0.2 episodes, p less than 0.05), but there was no effect on the frequency of episodes of silent ischemia (4.2 vs 3.4 episodes, NS). In patients with classic exertional angina, the addition of nifedipine had no effect on any measure of ambulatory ischemia. We conclude that patients with mixed angina are more likely to benefit symptomatically from the addition of nifedipine therapy than patients with classic exertional angina. The lack of a consistently preferential response to nifedipine in patients with mixed angina, however, suggests that episodic coronary vasoconstriction may not be the only mechanism responsible for ischemia in these patients, and/or that nifedipine may not necessarily provide additional therapeutic benefit beyond that conferred by a regimen of beta blockers and/or nitrates.

Adrenergic beta-Antagonists↗
PubMed1988

Postmyocardial infarction pain and infarct extension in the coronary care unit: role of two-dimensional echocardiography.

Recent data suggest that patients who manifest extension of their acute myocardial infarct have a worse prognosis than to those who do not have this complication and, if identified early, may be candidates for more aggressive intervention. Serial two-dimensional echocardiography was used to diagnose myocardial infarct extension in 33 consecutive patients and its sensitivity was compared with that of electrocardiography (ECG) and serum creatine kinase determination. Infarct extension was diagnosed clinically using ECG and enzymatic criteria. The echocardiograms were scored using a weighted regional scoring system, with each segment of the left ventricle ascribed a percent of the total left ventricular mass. Abnormal regions were summed to yield a percent asynergy. In the postinfarction period, 19 episodes of acute ischemia occurred; in 9 of these episodes clinical extension was confirmed, and in 7 of the 9 episodes echocardiographic extension was detected. In the patients in whom infarct extension was documented clinically, the mean asynergy score increased from a mean of 19.2 +/- 11.3% to 36.1 +/- 18.2% (p less than 0.01). Where no extension was detected, the asynergy score improved from the initial 31.5 +/- 24.1% to 28.3 +/- 21.9% (p less than 0.05). The extent of the change in echocardiographic wall motion abnormality was not predicted by the amount of creatine kinase reelevation. Electrocardiography alone failed to distinguish which episodes of ischemia represented infarct extension and which did not. Greater degrees of asynergy were associated with worse in-hospital mortality. Two-dimensional echocardiography is a useful method for detecting myocardial infarct extension providing a means of assessing functional impact and prognosis.

Adult↗
PubMed1988

Acute reduction in functional infarct expansion with late coronary reperfusion: assessment with quantitative two-dimensional echocardiography.

Reperfusion performed too late to salvage myocardium decreases chronic infarct expansion in experimental animals. However, the acute effects of delayed reperfusion are not known. Twenty-two dogs underwent 3 (n = 8), 4 (n = 8) or 6 h (n = 6) of circumflex artery occlusion followed by 3 h of reperfusion. Effects of reperfusion on diastolic expansion were assessed in two ways: 1) change in mean radius of curvature of the infarct segment, and 2) change in the ratio of the length of the diameter from the center of the infarct zone to the opposite wall (septal-lateral diameter) to the length of the diameter perpendicular to this (anteroposterior diameter). Effects on systolic expansion were examined with quantitative two-dimensional echocardiographic systolic thickening analysis. Delayed reperfusion produced an immediate decrease in diastolic infarct expansion. The ratio of septal-lateral/anteroposterior diameters, which had increased with occlusion from a preocclusion baseline of 0.98 +/- 0.06 to 1.13 +/- 0.08 (p less than 0.001), decreased with reperfusion to 1.02 +/- 0.07 at 15 min and 1.03 +/- 0.08 at 3 h of reperfusion (p = 0.001). This was due solely to a decrease in the septal-lateral diameter. The radius of curvature of the infarcted segment increased from 2.1 +/- 0.5 cm before reperfusion to 2.74 +/- 0.8 cm at 15 min and 2.6 +/- 0.85 cm at 3 h of reperfusion (p = 0.009). This occurred despite a significant (13.6%) decline in end-diastolic cavity area and is compatible with flattening of the reperfused infarct region. Systolic infarct expansion also improved slightly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Guidelines for optimal physician training in echocardiography. Recommendations of the American Society of Echocardiography Committee for Physician Training in Echocardiography.

Over the past few years, the clinical use of echocardiography has continued to expand. Echocardiographic techniques are used widely to define normal and abnormal cardiac anatomy, evaluate cardiac chamber sizes and dynamics, assess valvular and pericardial diseases, detect intracavitary masses, measure pressure gradients across discrete stenoses, determine flow volumes, detect and assess the severity of valvular regurgitation, demonstrate and quantitate intracardiac shunts, and measure the timing of cardiac events. These and related applications have led to the increasing use of echocardiography in the diagnostic evaluation of many cardiac disorders. Echocardiography requires considerable theoretical knowledge, technical skill and practical experience to be used in an optimal manner. Previous publications have suggested guidelines for physician training in the techniques of M-mode and 2-dimensional echocardiography. The clinical applications of echocardiography continue to grow, however, and Doppler techniques for evaluating blood flow have become an established component of the echocardiographic evaluation of many disorders. This article presents the current recommendations of the American Society of Echocardiography as to the background knowledge, the nature and amount of practical experience, and the type of training site that are optimal for the training of physicians who take responsibility for the conduct and interpretation of echocardiographic studies.

Cardiology↗
PubMed1987

Acute myocardial infarction: diagnostic and prognostic applications of two-dimensional echocardiography.

Now that we are entering an era when thrombolytic therapy and early invasive interventions appear to offer significant myocardium-sparing effects, it is important to attempt to exploit techniques that bear directly on the issue of anatomy to obtain an objective measure of infarct size and prognosis. Traditional tests for AMI were developed as diagnostic measures and cannot be expected to measure up to issues raised by modern therapy. Despite its pitfalls, echocardiography can be applied prognostically during the first few hours of AMI evolution to far more patients than can any other imaging technique. We believe that an adequate echocardiographic examination can be an important adjunct that should be used in the early risk assessment of any patient with AMI. Those patients with the greatest potential reversible myocardial damage are clearly the best candidates for aggressive interventions, particularly thrombolysis. For patients with small or no detectable regional wall motion abnormalities, a more conservative initial approach is in order.

Echocardiography↗
PubMed1986

In vivo prediction of the transmural extent of experimental acute myocardial infarction using contrast echocardiography.

Acute myocardial infarction progresses radially from endocardium to epicardium within the ischemic area. The amount of progression is highly variable, but depends largely on the transmural distribution of myocardial blood flow. Recent contrast echocardiographic observations indicate that slowly appearing low levels of contrast enhancement are often seen in the ischemic region, particularly in the epicardial level, and that ischemic regions which show these low levels of contrast have significantly more blood flow than those that do not. This study was designed to determine whether the transmural distribution of this delayed contrast enhancement can sufficiently discriminate between regions of high and low flow to serve as an in vivo predictor of the transmural extent of acute infarction. Twenty-four dogs had acute circumflex coronary ligation which was maintained for 6 hours. Contrast echocardiographic studies were performed at the level of the mitral chordae 2 hours after occlusion using a dilute hydrogen peroxide and blood solution as a contrast agent. Comparison was made with the pathologic infarct measured by triphenyltetrazolium chloride staining. The mean transmural extent of infarction ranged from 0 to 89% and was predicted in vivo by the transmural extent of the delayed contrast defect (r = 0.92; infarction [percent transmural] = 0.74 contrast [percent transmural] + 11%; SEE = 10%). Reproducibility for the transmural extent of delayed contrast defects was good (r = 0.89 to 0.98.) These data further support the concept that the transmural distribution of delayed contrast enhancement parallels blood flow and indicate that the mean transmural extent of acute infarction can be predicted in vivo 2 hours after coronary occlusion from the residual contrast defect.

Animals↗