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Biomedical subjects

A F Parisi

Publications and source records attributed to A F Parisi.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1986

Overestimation of infarct size by quantitative two-dimensional echocardiography: the role of tethering and of analytic procedures.

Analyses of regional left ventricular systolic wall motion or thickening overestimate infarct size. We used quantitative two-dimensional echocardiographic analysis of systolic thickening and contrast two-dimensional echocardiography to evaluate causes for that overestimation. The following possibilities were considered: "tethering," defined as dysfunction of contrast-enhancing myocardium adjacent to ischemic or contrast-negative regions, and the role of standard center of mass analysis algorithms, which may overestimate wall motion abnormalities because of the axis shift produced by simultaneous systolic expansion of the ischemic segment and systolic contraction of the nonischemic segment. In the short-axis view in 12 animals, the echo contrast defect (ECD) occupied 32 +/- 7% of the left ventricular circumference. Extent of dysfunction by the center of mass analysis was 39 +/- 5% of the left ventricular circumference and correlation with ECD size was .68 (SEE = 5.2%). Thus 8 +/- 6% of the circumference of the left ventricle was assessed to be dysfunctional yet enhanced with contrast. Tethering accounted for only half of this (4 +/- 4% of left ventricular circumference) and involved less than 1 cm on either side of the ECD. The remaining overestimation by the center of mass analysis correlated significantly (r = .89, p less than .01) with the amount of systolic expansion of the ECD. This expansion of the ECD (increase in angle subtended by the ECD of 11 +/- 8%) was produced by the systolic shift in the center of mass toward the dysfunctional segment from contraction of the opposite, nonischemic segment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Combination therapy with diltiazem and propranolol: precipitation of congestive heart failure.

Although congestive heart failure has been reported with the combination of a beta blocker and either verapamil or nifedipine, it has not previously been reported for combination therapy that includes diltiazem. The following case documents the occurrence of clinical congestive failure in a patient with baseline left ventricular dysfunction and severe angina pectoris. Although the patients had tolerated propranolol therapy for years without difficulty, and high-dose diltiazem monotherapy with an excellent clinical response, the combination of diltiazem and propranolol resulted in the development of congestive heart failure. Thus, although generally well tolerated, given the suitable scenario of reduced left ventricular function, the combination of diltiazem and a beta blocker may adversely affect left ventricular performance.

Angina Pectoris↗
PubMed1985

Serial studies of platelet factor 4 and beta thromboglobulin during exercise in patients with coronary artery disease.

In vivo activation of platelets can be accurately measured by radioimmunoassays of platelet factor 4 (PF4) and beta thromboglobulin (beta TG). Studies that attempt to correlate increases in PF4 and beta TG levels with exercise-induced myocardial ischemia have yielded conflicting results. To further examine the natural history of release of PF4 and beta TG we used a method of serial samplings of these proteins during and after exercise in nine normal subjects and 24 patients with coronary artery disease (CAD). Mean values for PF4 and beta TG at rest, during each stage, and immediately after treadmill exercise were the same for normal subjects and for patients with positive and negative responses to exercise-tolerance tests (ETTs). However, nonparametric analysis and regression equations disclosed differences in trends of PF4 level during exercise; PF4 levels increased in normal subjects during exercise, while patients with positive ETTs had no change in PF4 levels and patients with negative ETTs actually showed a decrease in PF4. This investigation confirmed that exercise-induced myocardial ischemia is not associated with platelet aggregation as manifested by the release of the platelet-specific proteins PF4 and beta TG. Statistical analysis suggested that prior reports of elevated levels of PF4 during exercise could have been caused by technical and methodologic difficulties that were associated with the collection and handling of the samples.

Adult↗
PubMed1985

Intraaortic balloon counterpulsation as a temporary support measure in decompensated critical aortic stenosis.

Intraaortic balloon counterpulsation was instituted in two adult patients whose condition was rapidly deteriorating because of critical decompensated valvular aortic stenosis. The acute hemodynamic effect of counterpulsation in these patients was compared with the effect of counterpulsation in three control patients with unstable angina and no aortic valve disease. Augmentation of aortic diastolic pressure was similar in both groups; however, in contrast to the patients with unstable angina, the patients with aortic stenosis had no decrease in left ventricular systolic pressure. Counterpulsation resulted in an increase in the transvalvular pressure gradient, which was associated with a slight increase in stroke volume. In both patients with aortic stenosis, the institution of counterpulsation resulted in marked clinical improvement, which facilitated successful valve replacement surgery. The benefit from counterpulsation in critically decompensated aortic stenosis appears to be derived almost entirely from augmentation of the diastolic coronary filling gradient. The improvement that results from counterpulsation suggests that ischemia is the major cause of decompensation.

Acute Disease↗
PubMed1985

Early loss of postextrasystolic potentiation in acutely ischemic myocardium: evaluation by contrast two-dimensional echocardiography.

Studies in animals with acutely ischemic hearts have suggested that postextrasystolic potentiation (PESP) may predict the viability of dysfunctional myocardium. Most of these data have been obtained with sonomicrometers and therefore the presence and extent of PESP throughout the entire region at risk has not been defined. In this study we used contrast two-dimensional echocardiography (2DE) to define region at risk in vivo, and then with quantitative 2DE we examined the proportion of the region at risk that demonstrated PESP, the degree of the potentiation, and the time course of this response. The region at risk was divided into a central (inner 50%) and two peripheral (25% each) ischemic zones. Adjacent contrast-enhanced myocardium was divided into near and far border zones that were equal in size to the adjacent peripheral ischemic zone. Systolic thickening was analyzed within each zone along multiple radii at 5, 30, and 120 min after coronary occlusion. PESP was absent in the central ischemic zone at all three times. In the peripheral ischemic zone at 5 min, a small amount of PESP was detected (-4.1% vs + 3.1% for nonpotentiated and potentiated thickening, respectively; p less than .01). At 30 min after occlusion, no potentiation was seen in the region at risk and PESP was confined to the contrast-enhanced near and far border zones. These findings persisted at 120 min. These data indicate that the response to PESP is localized to perfused myocardium by 30 min after acute occlusion. PESP is therefore of limited value in predicting the presence of ischemic, potentially viable myocardium early in the course of acute infarction.

Animals↗
PubMed1985

Superiority of combined diltiazem and propranolol therapy for angina pectoris.

Twenty-four patients with stable angina were evaluated in a 14 week crossover trial. A single-blind placebo period (baseline 1) was followed by two double-blind periods evaluating maximum tolerated doses of diltiazem (up to 360 mg daily) vs placebo. Over the next 1 to 4 weeks, propranolol was started and increased until clinically documented beta-blockade was achieved (baseline 2). The final phase consisted of a pair of evaluation periods comparing propranolol plus the maximum tolerated dose of diltiazem to propranolol and placebo. The daily rate of angina attack was 1.6 during baseline, was unchanged during placebo therapy, but fell during treatment with diltiazem to 0.6 (p less than .005). With the addition of diltiazem to propranolol, the angina rate was improved (0.3) compared with that with either propranolol alone (0.6) or propranolol and placebo (0.5) (p less than .01). Total exercise duration during baseline 1 was 360 sec and increased to 497 sec with diltiazem, 481 sec with propranolol, and 527 sec with the combination of diltiazem and propranolol. Two patients with reduced ejection fractions developed congestive heart failure with propranolol. The combination of diltiazem and propranolol similarly resulted in congestive heart failure in one patient who had tolerated both drugs alone.

Aged↗
PubMed1985

Non-Q wave perioperative myocardial infarction: assessment of the incidence and severity of regional dysfunction with quantitative two-dimensional echocardiography.

Since the widespread use of hypothermic potassium cardioplegia began, marked reductions in perioperative mortality and the rate of Q wave-associated myocardial infarctions have been noted. No study to date has evaluated whether there has been an equally dramatic improvement in the incidence of postoperative myocardial infarctions unassociated with Q wave development. We used a previously validated quantitative two-dimensional echocardiographic analytic algorithm to determine the incidence and severity of regional wall motion abnormalities (RWMAs) and first-pass radionuclide ventriculography to assess deterioration in global left ventricular function in the four following groups of patients (total n = 65): (1) those with peak postoperative creatine kinase (CK)-MB levels equal to or less than the mean value for patients undergoing coronary artery bypass surgery at our institution (n = 10), (2) those with CK-MB levels between the mean and 1 SD above the mean (n = 10), (3) those with peak CK-MB levels higher than 1 SD above the mean (n = 25), and (4) those with new pathologic Q waves on the postoperative electrocardiogram (n = 20). All patients had electrocardiograms without pathologic Q waves and normal wall motion and ejection fraction by contrast ventriculography before surgery. The incidence of postoperative RWMA by two-dimensional echocardiography for groups 1 through 4 was 0%, 20%, 55%, and 89%, respectively. Percent of abnormal left ventricular segments, wall motion scores, and the deterioration in left ventricular ejection fraction as assessed by radionuclide ventriculography were similar for patients with new RWMAs whether or not new Q waves developed (p = NS for all).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1985

Contrast echocardiographic estimation of regional myocardial blood flow after acute coronary occlusion.

Contrast echocardiography can predict pathologic area at risk during acute coronary occlusion. In this study we evaluated (1) whether the intensity and timing of contrast appearance in ischemic regions can provide a quantitative measure of residual myocardial perfusion, and (2) whether changes in these parameters observed after serial injections reflect changes in blood flow to acutely ischemic tissue. Supra-aortic hydrogen peroxide contrast echocardiography was performed in 12 consecutive dogs at 1, 20, and 120 min after acute circumflex coronary occlusion. Contrast enhancement was determined qualitatively with a segmental four-point scoring system based on the appearance time and peak perceived intensity of contrast enhancement and quantitatively with a computer algorithm designed to reflect these parameters. Comparison was made in each segment to concomitant radioactive microsphere blood flow. Qualitative scoring related systematically to normalized segmental blood flow (3+ = 93%; 2+ = 61%; 1+ = 32%; 0 = 18%; p less than .01 for each vs adjacent value), as did quantitative analysis including all segments (r = .78; p less than .01) and isolated to the ischemic region (flow = 1.13 intensity change +6.8%; r = .83, p less than .001). Changes in microsphere flow in ischemic regions between sequential observations were correlated with changes in qualitative score (r = .88, p less than .001) and results of quantitative analysis (r = 0.70, p less than .01). The amount of contrast enhancement can provide quantitative information about residual myocardial blood flow in ischemic regions and can also be used to track changing patterns of flow in vivo after acute coronary occlusion.

Animals↗
PubMed1984

Dissociation between two-dimensional echocardiographic left ventricular wall motion and myocardial salvage in early experimental acute myocardial infarction in dogs.

This study was designed to evaluate whether the effects of coronary reperfusion with or without a pharmacologic agent could be detected in the early hours after infarction by 2-dimensional (2-D) echocardiography applied in a manner analogous to its clinical use. Proximal left anterior descending coronary occlusion was performed in 24 dogs, and the dogs were then randomized into 3 groups. In group 1 (n = 8), coronary occlusion was maintained for 6 hours; in group 2 (n = 8), coronary occlusion was maintained for 2 hours and was followed by 4 hours of reperfusion; in group 3 (n = 8), 2 hours of coronary occlusion were followed by 4 hours of reperfusion but methylprednisolone (30 mg/kg intravenously) was also administered 15 minutes after coronary occlusion. At 6 hours, 2-D images were obtained through the closed chest wall and the percentage of the left ventricular wall motion abnormalities was determined at 4 short-axis levels. The mass at risk was defined by in vivo Monastral blue injection and infarction by triphenyltetrazolium chloride staining. The mass of necrosis was 74 +/- 4% (mean +/- standard error of the mean) of the mass at risk in group 1 and was smaller in groups 2 and 3, 44 +/- 6% and 35 +/- 4%, respectively (p less than 0.01). Percent necrosis of the left ventricle was 22 +/- 3% in group 1, 15 +/- 3% in group 2 (difference not significant) and 10 +/- 2% in group 3 (p less than 0.05 vs group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗