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Objectives The purpose of this study was to compare postoperative outcome in two groups of patients with chronic severe aortic regurgitation (AR): those operated on early and those operated on late according to the guidelines. Background The impact of earlier surgery for chronic severe AR as defined in guidelines has not been evaluated. Methods A total of 170 patients with chronic severe AR submitted to aortic valve replacement were prospectively followed up. Patients were divided in two groups depending on the clinical situation at the time of surgery. Group A were 60 patients who were operated on following guidelines advice of earlier surgery, and group B were 110 patients who were operated on late with regard to guideline recommendations. Results Follow-up was 10 ± 6 years (1 to 22 years). During follow-up 44 patients died, 7 patients (12%) from group A and 37 (37%) from group B (p = 0.001). The cause of death was non-cardiac in 11 patients, 2 (3%) in group A and 9 (8%) in group B. Cardiac deaths occurred in 33 patients, 5 (9%) from group A and 28 (28%) from group B (p = 0.002). Causes of death differed between groups A and B: heart failure or sudden death were significantly more frequent in group B (20 patients vs. 1 patient, p = 0.001). Overall survival in groups A and B was 90 ± 4% vs. 75 ± 8% at 5 years, 86 ± 5% vs. 64 ± 5% at 10 years, and 78 ± 7% vs. 53 ± 6% at 15 years, respectively (p = 0.009). Conclusions Early operation as defined in the guidelines improves long-term survival in patients with chronic AR.

Objectives We sought to assess the effect of glycoprotein (GP) IIb/IIIa blockade on myocardial platelet and polymorphonuclear leukocyte accumulation and on infarct size after coronary injury and transient coronary occlusion (CO) in pigs. Background It has been suggested that platelet GP IIb/IIIa blockade might reduce the severity of microvascular damage after reperfusion. Methods Sixteen thiopental-anesthetized, open-chest pigs, in whom platelets had been labeled with technetium-99m (99mTc) on the previous day, were submitted to catheter-induced left anterior descending coronary artery (LAD) injury followed by 55 min of CO and 5 h of reperfusion. Five minutes before reflow, the animals were blindly allocated to receive lamifiban (intravenous bolus of 250 μg/kg body weight and continuous infusion of 3 μg/kg per min) or saline. Results Lamifiban had a rapid and potent platelet anti-aggregatory effect, as demonstrated by significant prolongation of the bleeding time and profound (∼90%) inhibition of ex vivo platelet aggregation, and completely prevented the development of cyclic flow reductions of the LAD (0 vs. 5 ± 1, one of them followed by re-occlusion, in control animals, p = 0.005). However, compared with animals receiving placebo, those treated with lamifiban had a similar (p = NS) content of 99mTc platelets in the reperfused myocardium (288 ± 40% vs. 205 ± 27% of the value in the control region, respectively) and similar myeloperoxidase activity (0.50 ± 0.17 U/g vs. 0.47 ± 0.17 U/g, respectively) and infarct size (46.8 ± 12.0% vs. 49.8 ± 10.5% of the area at risk, respectively). Arteriolar platelet thromboemboli were very rarely seen on histologic analysis. Lamifiban did not modify platelet P-selectin expression in additional studies. Conclusions Platelet GP IIb/IIIa blockade has a potent antithrombotic effect at the culprit lesion, but does not significantly reduce the magnitude of microvascular platelet accumulation or myocardial damage after transient CO.

OBJECTIVESThe goal of this study was to investigate possible differences in thrombin generation or fibrinolytic capacity in patients with unstable angina (UA) or acute myocardial infarction (AMI) with or without recurrent angina at rest.BACKGROUNDAngina at rest in patients with AMI or UA is generally produced by a reduction in coronary flow, but it is unclear whether patients with or without this event differ in their thrombin generation or in their fibrinolytic capacities, which might influence the course of the culprit lesion.METHODSThrombin-antithrombin complex (TAT), D-dimer, fibrinogen and plasminogen activator inhibitor (PAI-1) antigen plasma levels were determined in 40 patients with AMI and in 23 with UA on admission, at 10 days and at three months.RESULTSFirst day values for TAT, fibrinogen and D-dimer were comparable in patients with AMI and in those with UA. At 10 days they increased significantly in each group, and at 3 months they decreased to a similar extent. First day PAI-1 levels, however, were highest in both groups and declined in AMI patients at 10 days and at three months, whereas they also decreased at 10 days in UA patients but not any further at three months. Ten patients with AMI (25%) and 12 with UA (52%) developed in-hospital angina at rest. First day values for TAT, fibrinogen and D-dimer were similar in patients with or without angina, but PAI-1 levels were higher in the former subset (p < 0.008). At 10 days, however, TAT (p < 0.013) and D-dimer (p < 0.013) were higher in patients who developed angina than in those who did not.CONCLUSIONSThe higher inhibition of fibrinolytic activity in the first day in patients with AMI or UA who will develop recurrent angina suggests that maintenance of a prothrombotic status may contribute to its mechanisms, perhaps by preventing passivation of the culprit thrombus/plaque. This is consistent with greater thrombin generation and greater levels of fibrynolitic products at 10 days observed in these patients compared with those who attain early stability.

OBJECTIVESWe sought to investigate the short-term prognostic value of the admission electrocardiogram (ECG) in patients with a first acute myocardial infarction (MI) without ST segment elevation.BACKGROUNDST segment depression on hospital admission predicts a worse outcome in patients with a first acute MI, but the prognostic information provided by the location of ST segment depression remains unclear.METHODSIn 432 patients with a first acute MI without Q waves or ≥0.1 mV of ST segment elevation, we evaluated the ability of the initial ECG to predict in-hospital death.RESULTSThe presence, magnitude and extent of ST segment depression were associated with an increased mortality, but the only electrocardiographic variable that was significant in predicting death after adjusting for baseline predictors was ST segment depression in two or more lateral (I, aVL, V5, or V6) leads (odds ratio 3.5, 95% confidence interval 1.2 to 10.6). Patients with lateral ST segment depression (n = 91, 21%) had higher rates of death (14.3% vs. 2.6%, p < 0.001), severe heart failure (14.3% vs. 4.1%, p < 0.001) and angina with electrocardiographic changes (20.0% vs. 11.6%, p = 0.04) than did the remaining patients, even though they had similar peak creatine kinase, MB fraction levels (129 ± 96 vs. 122 ± 92 IU/liter, p = NS). In contrast, ST segment depression not involving the lateral leads did not predict a poor outcome. Among patients who were catheterized, those with lateral ST segment depression had a lower left ventricular ejection fraction (57 ± 12% vs. 66 ± 13%, p = 0.001) and more frequent left main coronary artery or three-vessel disease than did the remaining patients (60% vs. 22%, p < 0.001).CONCLUSIONSIn patients with a first non–ST segment elevation acute MI, ST segment depression in the lateral leads on hospital admission predicts a poor in-hospital outcome.

Objectives. We analyzed the possible relation between the presence of a hospital admission delay (≥24 h), undue physical effort or recurrence of anginal pain, alone or in combination, with the development of free wall rupture (FWR), septal rupture (SR) or papillary muscle rupture (PMR) in patients with an acute myocardial infarction (AMI).Background. Physical activity as a trigger of FWR in AMI remains controversial, and its contribution to SR or PMR remains unknown. Moreover, the role of ischemia or reinfarction as an additional cause of rupture has not been explored.Methods. The incidence of hospital admission delay ≥24 h with maintenance of some ambulatory activity and the incidence of postinfarction angina were analyzed in consecutive patients with a first AMI with (n = 225) or without rupture (n = 1,012 [control group]) over different time periods.Results. An admission delay ≥24 h occurred in 27 (27.6%) of 98 patients with FWR, 47 (47.0%) of 100 with SR and 14 (51.9%) of 27 with PMR but in only 81 (8%) of 1,012 control patients (p < 0.0001). Information on undue in-hospital effort preceding rupture was available for 111 patients and was present in 17 (32.7%) of 52 with FWR, 9 (18.4%) of 49 with SR and 3 (30%) of 10 with PMR versus only 76 (7.5%) of 1,012 control patients (p < 0.001). Information on postinfarction anginal pain was available for 114 patients with rupture and occurred in 30 (56.6%) of 53 with FWR, 30 (60%) of 50 with SR and 4 (36.4%) of 11 with PMR versus 120 (11.9%) of 1,012 control patients (p < 0.0001). Mean age and incidence of male gender, hypertension, absence of heart failure, single-vessel disease or occlusion of the infarct-related artery were comparable among the groups with FWR, SR or PMR.Conclusions. Delayed hospital admission or undue in-hospital physical activity appears to increase the risk of rupture in patients prone to this complication (i.e., a first transmural AMI, absence of overt heart failure and advanced age); recurrence of ischemia/infarction emerges as a potential additional trigger in a proportion of these patients.

Objectives. We attempted to demonstrate that simultaneous dipyridamole administration and maximal subjective exercise in patients who are unable to achieve a good exercise level can improve the diagnostic efficacy of technetium-99m methoxy isobutyl isonitrile (99mTc-MIBI) myocardial single-photon emisson computed tomography (SPECT).Background. The results of myocardial perfusion scintigraphy are unsatisfactory if the level of exercise achieved by the patient is insufficient. The use of dipyridamole with maximal subjective stress testing has been shown to improve the quality of the thallium-201 myocardial perfusion images, but there are no studies demonstrating that this combination improves the diagnostic accuracy of myocardial perfusion SPECT.Methods. Two hundred thirty-one consecutive patients, without a previous myocardial infarction, were classified into three groups: group 1, 91 patients with an adequate exercise test; group 2, 68 patients with an inadequate exercise test; group 3, 72 patients with an inadequate exercise test who then received intravenous dipyridamole (0.56 mg/kg body weight over 4 min) simultaneously with exercise.Results. Results for sensitivity (89%) and negative predictive value (83%) in group 3 were significantly better than those in group 2 (71% [p = 0.03] and 56% [p = 0.002], respectively) and not significantly different from those in group 1. The polar maps of 20 patients studied with and without dipyridamole at the same exercise level revealed a significantly greater extent of ischemia in each territory and in a global assessment (19 + 20% vs. 8 + 11%, p < 0.0001) when dypiridamole was administered during physical exercise.Conclusions. Intravenous dipyridamole administration during exercise testing is advisable in all patients who are unable to achieve an adequate exercise level. This approach permits physicians to avoid missing ergometric information while optimizing myocardial SPECT results.(J Am Coll Cardiol 1997;29:531–6)

Objectives. This study sought to assess the reliability of biplanar transesophageal echocardiography in the diagnosis of ascending aortic dissection and to test the utility of M-mode information in the differential diagnosis of ascending aortic ultrasound artifacts and intimal flap images. Background. Transesophageal echocardiography is a useful technique in the diagnosis of aortic dissection. However, ultrasound artifacts in the ascending aorta are an important limitation. Methods. Transesophageal echocardiography was performed in 132 consecutive patients with clinically suspected aortic dissection. Two-dimensional and M-mode echocardiography and color Doppler were used to diagnose intimal flap and artifact images. Diagnoses were validated either anatomically or with reference techniques. Results. The sensitivity and specificity of transesophageal echocardiography in the diagnosis of ascending aortic dissection were 96.8% and 100%, respectively. Ninety-three artifacts were observed in 56 (55%) of 101 patients without ascending aortic dissection. Two-dimensional echocardiography easily identified 74 artifacts (80%). Color Doppler showed no ascending flow abnormalities in 71% of artifact images. M-mode echocardiography showed three location and mobility artifact patterns related to the posterior wall of the aorta or the right pulmonary artery. In contrast, intimal flap movement showed no relation to the aortic wall movement in 25 cases (83%). Blind analysis of transesophageal echocardiographic study tapes underlined the utility of M-mode in the differential diagnosis. Ranges of sensitivity, specificity and positive predictive value (established by including doubtful results as either positive or negative) improved from 87.1–93.5% to 93.5- to 96.8%, from 85.1–94.1% to 99–100% and from 65.9–81.8% to 96.8–100%, respectively, with the inclusion of M-mode data. Conclusions. Biplanar transesophageal echocardiography permits reliable diagnosis of ascending aortic dissection. Ultrasound artifacts are common, but assessment of the location and mobility of intraluminal images by M-mode echocardiography definitely improves diagnostic accuracy.

Objectives. This study assessed the efficacy of oral etilefrine (10 mg three times a day) in preventing a positive response to head-up tilt testing. Background. Previous reports have suggested that oral etilefrine can be effective either in preventing a positive response to head-up tilt testing or in reducing syncopal recurrences in patients with vasovagal syncope. Up to now most studies assessing drug therapy in these patients have been uncontrolled. Methods. This was a randomized double-blind crossover study of etilefrine versus placebo in 30 consecutive patients with syncope and a baseline positive head-up tilt test. After the first test, patients had no treatment for 3 days and were randomized to receive etilefrine or placebo for 4 additional days. They underwent tilt testing under treatment and again after 3 days of washout; they then received the alternative treatment for 4 days, and a third test was performed. Results. Head-up tilt test results were negative in 13 (43%) patients with etilefrine and 15 (50%) with placebo (p = NS). Therefore, the statistical power of the study was only 10%. The rate of positive responses decreased with repeated testing irrespective of the assigned treatment: A positive response was obtained during the second head-up tilt test in 20 patients (10 with placebo, 10 with etilefrine) but in only 12 during the third (7 with etilefrine, 5 with placebo) (p Conclusions. Oral etilefrine (10 mg three times a day) was not superior to placebo in preventing a positive response to head-up tilt testing. Despite a low statistical power, the high rate of negative response with placebo (50%) suggests that controlled trials are needed to assess the real efficacy of any treatment in patients with vasovagal syncope.

To evaluate the prognostic role of combined cardiac studies (submaximal exercise test, thallium-201 scintigraphy, radionuclide exercise ventriculography, two-dimensional echocardiography, Holter monitoring and cardiac catheterization) in patients with a first acute myocardial infarction without complications during hospital admission, 115 consecutive patients aged less than 65 years were prospectively evaluated. The studies were carried out before hospital discharge and the patients were then clinically followed up for 12 months. During the follow-up period, 69 patients (60%) developed complications, which were severe in 23 (20%). Half of all complications and 70% of severe complications developed during the 1st follow-up month. Logistic regression analysis disclosed that the combination of studies with the highest predictive power for complications (probability of complications 99%) and severe complications (probability of severe complications 95%) was the association of exercise test + thallium-201 + echocardiogram. Four decision models (exercise test + echocardiography, exercise test + radionuclide ventriculography, thallium-201 scintigraphy + echocardiography, thallium-201 scintigraphy + radionuclide ventriculography) allowed the stratification of all patients in a particular risk category (high, intermediate or low). The best decision model was the association of thallium-201 scintigraphy + radionuclide ventriculography (probability of complications if both tests were positive 84%; probability of absence of severe complications if both tests were negative 88%), but there were no significant differences with the other models. Any association of a test detecting residual ischemia or functional capacity, or both (exercise test or thallium-201) and a test assessing ventricular function (echocardiography or radionuclide ventriculography) results in significant prognostic information in patients with an uncomplicated first acute myocardial infarction. Additional cardiac catheterization does not improve the predictive power of noninvasive studies, which should ideally be performed before hospital discharge because most complications develop during the 1st follow-up month.

The purpose of this study was to compare postoperative outcome in two groups of patients with chronic severe aortic regurgitation (AR): those operated on early and those operated on late according to the guidelines.The impact of earlier surgery for chronic severe AR as defined in guidelines has not been evaluated.A total of 170 patients with chronic severe AR submitted to aortic valve replacement were prospectively followed up. Patients were divided in two groups depending on the clinical situation at the time of surgery. Group A were 60 patients who were operated on following guidelines advice of earlier surgery, and group B were 110 patients who were operated on late with regard to guideline recommendations.Follow-up was 10 +/- 6 years (1 to 22 years). During follow-up 44 patients died, 7 patients (12%) from group A and 37 (37%) from group B (p = 0.001). The cause of death was non-cardiac in 11 patients, 2 (3%) in group A and 9 (8%) in group B. Cardiac deaths occurred in 33 patients, 5 (9%) from group A and 28 (28%) from group B (p = 0.002). Causes of death differed between groups A and B: heart failure or sudden death were significantly more frequent in group B (20 patients vs. 1 patient, p = 0.001). Overall survival in groups A and B was 90 +/- 4% vs. 75 +/- 8% at 5 years, 86 +/- 5% vs. 64 +/- 5% at 10 years, and 78 +/- 7% vs. 53 +/- 6% at 15 years, respectively (p = 0.009).Early operation as defined in the guidelines improves long-term survival in patients with chronic AR.

Objectives The goal of this study was to assess whether selectin blockade reduces myocardial platelet deposition and platelet-mediated injury after transient ischemia. Background Selectins participate in platelet adhesion to reperfused endothelium. Methods Thiopental-anesthetized, open-chest pigs were subjected to mechanical injury of the left anterior descending coronary artery followed by a 48-min occlusion and 2 (n = 20) or 4 (n = 16) h of reperfusion. Fifteen minutes before occlusion, animals were blindly allocated to receive a continuous intravenous infusion of the selectin blocker fucoidan (30 μg/kg/min, plus a 1-mg/kg bolus in the latter group) or saline. In isolated rat hearts infused with thrombin-activated platelets, the effects of fucoidan (30 μg/ml) administered during reperfusion after 40 min of global ischemia were also analyzed. Results Fucoidan did not prevent the development of cyclic reductions in coronary flow, but reduced the content of 99mTc-labeled platelets in reperfused myocardium after 2 h of reperfusion (23.4 ± 3.3 vs. 42.1 ± 8.3 × 106platelets/g in treated and untreated animals, p = 0.03) and attenuated the impairment in the coronary flow reserve and reduced infarct size after 4 h (53 ± 2% vs. 73 ± 5% of the ischemic region, respectively, p = 0.003). Treated animals showed a trend toward less neutrophil infiltration early after reperfusion, but not after 4 h. In isolated hearts, fucoidan improved functional recovery and reduced coronary resistance and lactate dehydrogenase release, lacking any beneficial effects if given in the absence of platelets. Conclusions The results suggest that selectin-dependent adhesion is a prominent mechanism of platelet deposition in reperfused cardiac microvessels and highlight its potential as a therapeutic target in patients with acute myocardial infarction.

ObjectivesThe purpose of the study was to analyze the factors that favor the occurrence of sustained monomorphic ventricular tachycardia in the early phase ( I: 63% vs. 30%, p < 0.05), higher CK-MB activity (430 ± 260 IU/liter vs. 242 ± 176 IU/liter, p < 0.01) and higher arrhythmia recurrence rate (31% vs. 4%, p < 0.01). During the follow-up period, 5 (42%) of 12 survivors in the sustained monomorphic ventricular tachycardia group died of cardiac-related causes. Recurrence of ventricular tachycardia was seen in two patients (17%).ConclusionsSustained monomorphic ventricular tachycardia during the first 48 h of myocardial infarction is a sign of extensive myocardial damage and an independent predictor of in-hospital mortality.

Objectives.This study was designed to determine the efficacy of intravenous amiodarone in the management of recent-onset atrial fibrillation.Background.The optimal approach for acute atrial fibrillation has not been established. Amiodarone is a unique antiarrhythmic agent with activity in both supraventricular and ventricular tachyarrhythmias, but its value for the restoration of sinus rhythm in patients with recent-onset atrial fibrillation has not been demonstrated.Methods.Sample size was calculated to detect a 25% increase in reversion rate with amiodarone with a statistical power of 80%. One hundred consecutive patients with recent-onset ( 100 beats/min. Amiodarone and digoxin blood levels were determined. Both groups were homogeneous regarding underlying heart disease, time from onset to treatment, initial ventricular rate and left atrial size.Results.By the end of the 24-h treatment period, 34 patients (68%, 95% confidence interval [CI] 53% to 80%) in the amiodarone group and 30 (60%, 95% CI 45% to 74%) in the control group had returned to sinus rhythm (p = 0.532). Mean times (±SD) of conversion were 328 ± 335 and 332 ± 359 min, respectively (p = 0.957). Among patients who did not convert to sinus rhythm, treatment with amiodarone was associated with a slower ventricular rate (82 ± 15 beats/min in the amiodarone group vs. 91 ± 23 beats/min in the control group, p = 0.022). After restoration of sinus rhythm, atrial fibrillation recurred during a 15-day follow-up period in 4 (12%) of 34 patients (95% CI 3% to 27%) in the amiodarone group and in 3 (10%) of 30 (95% CI 2% to 26%) in the control group (p = 0.861).Conclusions.Intravenous amiodarone, at the doses used in this study, produces a modest but not significant benefit in converting acute atrial fibrillation to sinus rhythm.

Autonomic innervation of the coronary arteries is thought to intervene in the genesis of coronary vasospasm, We assessed the potential effect of selective coronary denervation in the inhibition of vasospasm. Chronic sympathetic and parasympathetic denervation was provoked by topical application of phenol to the proximal LAD in 20 pigs through a lateral thoracotomy. Two weeks later, we performed an midsternal thoracotomy. Heart rate, aortic and ventricular (LV) pressure, LV dP/dt, coronary blood flow (CBF) at the LAD, and 32–channel epicardial ST segment mapping were monitored during every MCH application. Phenol-induced coronary adrenergic and cholinergic denervation was confirmed by histofluorescence and cholinesterase staining, Isolated LAD rings of 5 phenol-denervated pigs were studied to confirm smooth muscle integrity, Application of MCH to control pigs (n = 10) induced an statistically significant fall in CBF (75 ± 19%) accompanied by electrical and mechanical signs of ischemia: mean ST segment elevation on the epicardial electrograms of 9,7 ± 4.7 mV, a drop in systolic LV pressure (-20 ± 8.4 mmHg) and a decrease in LV dP/dt (-404 ± 203 mmHg/s). There were no changes in heart rate. The parameters returned to normal values after 5 to 8 min. As compared to controls, phenol treated pigs showed a significant attenuation ofthe fall in CBF (25 ± 17%), lesser ST segment elevation (2.4 ± 2.1 mV), a lower drop in LV pressure (-8 ± 2.3 mmHg), and a smaller decrease in LV dP/dt (-167 ± 104 mmHg/s). Coronary angiography performed in 6 additional pigs evidenced that the coronary spasm occurred at the site of MCH exposure. Isolated LAD rings of phenol treated pigs constrict after incubation with endothelin-1 indicating preserved vascular smooth muscle function. In 5 control pigs, a second application of MCH after muscarinic receptor blockade with atropine (0.4 mg/kg iv.) resulted in complete abolition of the vasospasm confirming that vasospasm was mediated by the muscarinic receptor stimulation. In conclusion, pericoronary autonomic denervation protects against coronary constriction induced by direct muscarinic receptor stimulation with methacholine in situ the pig heart.

Prompt inhibition of platelet aggregation is important in acute coronary syndrome and before an intervention procedure. To determine whether a single low dose of iv aspirin inhibits platelet aggregation, twenty-seven healthy volunteers (7 F and 20 M), mean age 43.5 years, were randomized double-blind to a single iv low dose of aspirin DL-Iysine (L-ASA) equivalent to 2 mg/kg of aspirin, high dose (H-ASA) equivalent to 10 mg/kg, or placebo (PI). Platelet aggregation were performed before and 1 hand 24 h after drug administration, in whole blood (WB) using electrical impedance and in platelet-rich plasma (PRP) by optical light transmittance. Baseline WB platelet aggregation (Col 3 μg/mI) was the same with L-ASA, H-ASA and PI (24 ± 5, 23 ± 3 and 24 ± 4rl respectively) and decreased significantly more with L-ASA and H-ASA than with PI after 1 h.(17 ± 6, 15 ± 7 and 21 ± 5Ω p l 0.0l)and 24 h(17 ± 7, 16 ± 6 and 25 ± 4Ω P l 0.01). Results in PRP were similar: PR Poptical aggregation (%) Before AfterASA 1 h. 24 h ADP (5/LM): L-ASA 73 ± 21 50 ± 14 * 45 ± 15 * H-ASA 65 ± 23 54 ± 17 * 52 ± 16 * PI 69 × 18 72 ± 22 69 ± 14 Col (3 /Lg/ml): L-ASA 64 ± 19 33 ± 13 * 36 ± 18 * H-ASA 60 ± 16 32 ± 17 * 34 ± 14 * PI 55 ± 13 56 ± 18 57 ± 14 * p l 0.001 (ANOVA test) respect to PI and the baseline values No differences in response were observed between the two doses of aspirin and no significant changes occurred between 1 and 24 hours in any group. Effective inhibition of platelet aggregation is thus achieved within 1 hour after the administration of low-dose 2 mg/kg of ivaspirin.

Coronary ligature with minimal intimal injury reproduces only in part acute coronary syndrome, in which reperfusion occurs through an extensively damaged artery. To analyze the influence of coronary endothelial injury (El) on PMN leukocyte accumulation and infarct size, 48 pigs were allocated to catheterization and endothelial denudation of the LAD or to no intervention immediately before a 48 min coronary occlusion and 6 h of reperfusion. Ninety min before they had received aspirin (ASA, 250 mg e.v.), or placebo (2 × 2 factorial design). Twelve animals presented reocclusion and were excluded for subsequent analysis, 2 of them receiving ASA and 10 not (p l 0.05). In the remaining pigs, blood flow (ml/[min.g]) in the area at risk was similar in those with than in those without EI. 30 min (2.2 ± 0.3 vs 2.3 ± 0.4) and 5 h (1.4 ± 0.2 vs 1.4 ± 0.2) after reflow. and was not modified by ASA. Infarct size (% of the area at risk, TIC reaction) was greater in pigs with EI. A significant interaction (p = 0.03) between El and ASA was detected, El being associated with larger infarcts in animals receiving placebo, but not in those receiving ASA: No EI (n = 18) EI (n = 18) p value Placebo (n = 18) 11 ± 4 36 ± 7 0.006 ASA (n = 18) 22 ± 6 20 ± 6 NS Myocardial content of PMNs (quantitative histology) in the area at risk was higher in animals with than in those without El (mean scores 4.9 ± 0.6 vs 3.0 ± 0.6, p = 0.04), and was not modified by ASA. In 12 additional experiments with 30 min coronary occlusion (no infarct), the content of Tc99 labeled PMNs in the area at risk was significantly increased in pigs with El (144 ± 23% of control myocardium), but not in those without (p = 003). Thus, El at the site of a transient coronary occlusion increases myocardial PMN content and necrosis. ASA reduces reocclusion rate and limits the deleterious effect of EI on infarct size in animals without reocclusion. This effect could be due to impared PMN-platelet cooperation, or to a direct effect of ASA on function of adhered PMNs.

Thirteen patients with tuberculous pericarditis (12 men and 1 woman aged 13 to 70 years [mean 41]) were identified in a group of 294 patients consecutively admitted for primary acute pericardial disease. The diagnosis was made by the following studies: sputum culture (n = 4), culture of pericardial fluid obtained by pericardiocentesis (n = 3), histologic study and culture of pericardial biopsy (n = 3), lymph node biopsy (n = 2) and plenral biopsy (n = 1). Clinical presentation was remarkably variable: four patients had an acute, apparently self-limited course, one had relapsing tamponade, four had tamponade effectively treated with pericardiocentesis and four had toxic symptoms with persistent fever. The interval from hospital admission to diagnosis ranged from 1 to 14 weeks (mean 5.2). Constrictive pericarditis developed in six patients and effusive-constrictive pericarditis in one; all seven required pericardiectomy 2 to 3.5 months after admission. No patient died.It is concluded that 1) tuberculous pericarditis has a variable clinical presentation and therefore it should be considered in the evaluation of all instances of pericarditis without a rapidly self-limited course; 2) the diagnosis should be based only on objective data obtained with a systematic study protocol; 3) early definitive diagnosis is still difficult to achieve; and 4) development of subacute constrictive pericarditis requiring pericardiectomy is common.

Objectives.Our aim was to use noninvasive studies early after infarction to assess medium-term prognosis in patients with a first uncomplicated myocardial infarction.Background.Although the use of early postinfarction assessment to gauge short-term prognosis in myocardial infarction is well established, there have been few comprehensive evaluations of noninvasive methods for assessing medium- and long-term prognosis.Methods.We prospectively studied 115 consecutive patients

Objectives. This study sought to evaluate the effects of prolonged rest and blood pressure control on survival of patients in whom left ventricular free wall rupture (LVFWR) was strongly suspected. Background. Left ventricular free wall rupture in myocardial infarction is often fatal, and only a few patients may undergo operation. However, survival without surgical repair has not yet been evaluated. Methods. Eighty-one consecutive patients with a first transmural acute myocardial infarction in Killip class I or II who presented with acute hypotension due to cardiac tamponade, with electromechanical dissociation (EMD) in 72, were prospectively evaluated. Patients with early recovery were managed with prolonged bed rest and blood pressure control with beta-blockade as tolerated. Results. Forty-seven patients died within 2 h of acute tamponade, and autopsy in 21 showed LVFWR in all. In 15 others, an emergency surgical repair resulted in 2 survivors. The remaining 19 patients, 10 with EMD, had early recovery with dobutamine and colloid solution, and 15 required pericardiocentesis. Shortly thereafter, these 19 patients still showed a paradoxic pulse ≥20 mm Hg, relevant pericardial effusion (24 ± 7 mm [mean ± SD]) and comparable elevation of right and left ventricular filling pressures (15.8 ± 3.9 and 15.9 ± 3.8 mm Hg, respectively). Subsequent management included bed rest (8.2 ± 4.8 days) and control of systolic blood pressure (≤120 mm Hg) with beta-adrenergic blocking agents as tolerated (n = 12). Four patients died, and autopsy in three revealed a rupture that was sealed in two. A sealed rupture was also seen at thoracotomy in 2 other patients who, like the remaining 13, survived for 52.5 ± 35.2 months. Conclusions. Long-term survival of selected patients with prompt hemodynamic recovery after LVFWR is possible without surgical repair. Prolonged bed rest and blood pressure control are likely to contribute favorably to their initial outcome. (J Am Coll Cardiol 1997;29:512–8)

Objectives.We attempted to ascertain whether cardiac index can be directly estimated from Doppler mean velocity.Background.Although diverse Doppler echocardiographic methods have been described for cardiac output quantification, they are not widely used in clinical practice. Cross-sectional area measurement has been identified as the main source of error in flow volume quantification.Methods.A three-phase study by Doppler echocardiography was conducted in 306 patients. In phase I, the normal mean velocity ratio of the left and right ventricular outflow tracts was established in 170 normal subjects. In phase II, cardiac index, calculated as the product of aortic annular area index by mean velocity (conventional method), and mean velocity determined in the left ventricular outflow tract and ascending aorta by pulsed and continuous wave Doppler, respectively, were correlated with thermodilution cardiac index in 66 patients. In phase III, the accuracy of the regression equations obtained was prospectively assessed in an additional 70 patients.Results.The normal left/right ventricular outflow tract mean velocity ratio by pulsed wave Doppler was 1.1 ± 0.1. Cardiac index (CI) calculated by the conventional method and thermodilution (TD) showed acceptable correlation (r = 0.90, CITD= 1.20 CIPWD+ 357; r = 0.86, CITD= 0.90 CICWD+ 262) for pulsed (PWD) and continuous wave (CWD) Doppler, respectively, but with systematic underestimation (−28 ± 13%, p < 0.01) by pulsed wave Doppler. Mean velocity (MV) showed excellent correlation with the thermodilution cardiac index (r = 0.97, CITD= 172 MVPWD−172; r = 0.93, CITD= 129 MVCWD−255). When these regression equations were prospectively applied, better agreement with the thermodilution cardiac index was obtained by pulsed wave Doppler directly from mean velocity (SD 240 ml/min per m2) than when aortic annular area was considered in the calculation (SD 428 ml/min per m2). Similar results were obtained by continuous wave Doppler (SD 433 vs. 599 ml/min per m2) but with less accuracy.Conclusions.Left ventricular outflow tract mean velocity determined by pulsed wave Doppler permits easy, accurate cardiac index quantification in the absence of left ventricular outflow abnormalities. The simplicity of this method enhances its clinical applicability in noninvasive monitoring of cardiac index.