Prognosis of acute myocardial infarction in the thrombolytic era: medical evaluation is still valuable.

BACKGROUND: Modern and sophisticated technology for the management of myocardial infarction has progressively devalued medical evaluation. HYPOTHESIS: This study was undertaken to assess the importance of the findings of medical evaluation at hospital presentation, in patients with acute myocardial infarction. METHODS: Data from 590 thrombolytic-treated myocardial infarction patients were analyzed. The patients were grouped according to their clinical status on arrival at hospital. A modified Forrester classification--subset II was divided according to the absence (IIa) or presence (IIb) of symptoms--was applied. Short- (14 days) and long-term (up to 10 years) survival was analyzed and 19 independent variables were included in the multivariate models. RESULTS: Short-term survival was 95.6% for subset I, 83.3% for subset IIa, 60% for subset IIb, 54.6% for subset III, and 34.8% for subset IV (P<0.001). By multiple regression analysis, lower clinical subsets (P<0.001), fewer coronary arteries with disease (P=0.006), younger age (P=0.014), absence of reinfarction (P=0.034), longer interval between streptokinase infusion and coronary arteriography (P=0.016), and higher left ventricular ejection fraction (P=0.037) demonstrated significant and independent correlation with short-term survival. Long-term survival for the total population was 71+/-3.6% for subset I, 54.4+/-8.5% for subset IIa, 20.8+/-9.4% for subset IIb, 54.5+/-15% for subset III, and 0% for subset IV (P<0.001). Using Cox regression analysis, lower clinical subsets (P<0.001), younger age (P<0.001), higher global left ventricular ejection fraction (P<0.001), and fewer coronary arteries with disease (P=0.021) correlated independently and significantly with long-term survival. When excluding data from patients who died before the short-term follow-up (n=532), lower clinical subsets remained an important predictor of long-term survival (P<0.001). CONCLUSION: Clinical classification at hospital presentation is a powerful predictor of short- and long-term survival post-myocardial infarction.

Effect of simvastatin on monocyte adhesion molecule expression in patients with hypercholesterolemia.

Increased monocyte adherence to the vessel wall is one of the earliest events in atherosclerosis. The mechanism by which hypercholesterolemia causes alterations in endothelial adhesiveness for monocytes is unclear. This study sought to determine if monocyte adhesion molecule expression is affected by low-density lipoprotein (LDL)-cholesterol levels. Patients with hypercholesterolemia and stable coronary artery disease were compared with those without major cardiovascular risk (control). Patients with hypercholesterolemia were treated with simvastatin 20--40 mg/day for 8--10 weeks. Blood samples were examined with flow cytometry assays at baseline and after cholesterol-lowering therapy. Monocyte CD11b and CD14 adhesion molecule expression, measured as fluorescence intensity, were significantly (P<0.0001) higher in hypercholesterolemic patients before the study (176.9+/-9.8 and 138.0+/-4.8, respectively) when compared with that in control subjects (97.2+/-8.1 and 84.0+/-6.4, respectively). Both decreased markedly with treatment: to 118.8+/-6.9 and 103.1+/-3.9, respectively. Monocyte L-selectin expression was significantly lower in patients with hypercholesterolemia before treatment (43.0+/-3.0) when compared with control subjects (79.9+/-2.7), and it increased markedly with treatment (54.2+/-2.5). LDL levels correlated directly with both CD11b and CD14 expression and correlated inversely with L-selectin expression. These data show that hypercholesterolemia affects monocyte adhesion molecule expression which, in turn, decreases with statin-induced plasmatic cholesterol reduction. Such perturbations in monocyte function likely represent a proinflammatory response to hypercholesterolemia and may have a role in the early progression of atherogenesis.

Trends in the risk of mortality due to cardiovascular diseases in five Brazilian geographic regions from 1979 to 1996.

OBJECTIVE - To analyze the trends in risk of death due to cardiovascular diseases in the northern, northeastern, southern, southeastern, and central western Brazilian geographic regions from 1979 to 1996. METHODS - Data on mortality due to cardiovascular, cardiac ischemic, and cerebrovascular diseases in 5 Brazilian geographic regions were obtained from the Ministry of Health. Population estimates for the time period from 1978 to 1996 in the 5 Brazilian geographic regions were calculated by interpolation with the Lagrange method, based on the census data from 1970, 1980, 1991, and the population count of 1996, for each age bracket and sex. Trends were analyzed with the multiple linear regression model. RESULTS - Cardiovascular diseases showed a declining trend in the southern, southeastern, and northern Brazilian geographic regions in all age brackets and for both sexes. In the northeastern and central western regions, an increasing trend in the risk of death due to cardiovascular diseases occurred, except for the age bracket from 30 to 39 years, which showed a slight reduction. This resulted from the trends of cardiac ischemic and cerebrovascular diseases. The analysis of the trend in the northeastern and northern regions was impaired by the great proportion of poorly defined causes of death. CONCLUSION - The risk of death due to cardiovascular, cerebrovascular, and cardiac ischemic diseases decreased in the southern and southeastern regions, which are the most developed regions in the country, and increased in the least developed regions, mainly in the central western region.

Effect of cholesterol lowering treatment on positive exercise tests in patients with hypercholesterolaemia and normal coronary angiograms.

AIM: To assess the impact of cholesterol lowering on positive exercise stress tests in hypercholesterolaemic patients with normal coronary angiograms. METHODS: 43 non-diabetic patients aged 43-61 years, with total serum cholesterol concentrations of more than 7.75 mmol/l, positive exercise tests, and normal coronary angiograms, were started on the American Heart Association step 1 diet. After 12 weeks these patients were randomly assigned to treatment for another 16 weeks with the diet alone (diet group, n = 20) or with the diet plus lovastatin or simvastatin (statin group, n = 23). After this 28 week run in period, statins were withdrawn and lipid profile tests and exercise tests were done and repeated 20 weeks later. RESULTS: At week 28, the statin group but not the diet group had significant reductions from baseline (week 12) in plasma total cholesterol (p < 0.0001), low density lipoprotein (p < 0.0001), and triglyceride (p < 0.0001). The number of patients with positive exercise tests decreased from 23 to three in the statin group and from 20 to 15 in the diet group (p = 0.01). After the final 20 weeks without statins, lipid profiles returned to baseline levels in all 17 patients remaining in the statin group, and exercise tests were again positive in 15 of these patients. CONCLUSIONS: In hypercholesterolaemic patients with normal coronary arteries, cholesterol lowering treatment reduces myocardial ischaemia, as shown by the beneficial effects on exercise testing.

Sinus bradycardia as a predictor of right coronary artery occlusion in patients with inferior myocardial infarction.

Differentiation of right coronary artery (RCA) from left circumflex artery (LCxA) occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction (IMI). We studied 133 patients with IMI, 92 patients with RCA occlusion and 41 patients with LCxA occlusion. Risk factors such as previous MI, arterial hypertension, diabetes, smoking, and dislipemia, were similar for RCA and LCxA occlusions. Patients with RCA occlusion had a higher incidence of isolated IMI than patients with LCxA occlusion, 50% vs. 17%, respectively (P<0.001). Arterial hypotension was more prevalent (P<0.05) among patients with RCA (18%) rather than those with LCxA occlusion (2%). RCA occlusion presented an association with sinus bradycardia, an association not observed with LCxA occlusion (15% vs. 0%, respectively; P<0.01). Total atrioventricular block was only present among patients with RCA (18%). Proximal occlusions of the RCA presented lower heart rates (sinus bradycardia) than medial and distal occlusions (13% vs. 1% and 1%, respectively; P<0.0001 and P<0.001). Therefore, regarding patients with IMI: (1) sinus bradycardia is more frequent when the infarct-related artery is the RCA; (2) proximal occlusions of the right coronary predispose low heart rates; and (3) occlusion of the LCxA rarely induces sinus bradycardia.

Early infarct artery collateral flow does not improve long-term survival following thrombolytic therapy for acute myocardial infarction.

It is known that acutely developed collaterals can prevent the onset of acute myocardial infarction (AMI) in the presence of a total coronary occlusion. However, there still is controversy concerning long-term follow-up of coronary collateral circulation to the infarct-related artery. In this study we analyze the prognostic role of collateral flow (degrees 0 to 3) as well as anterograde flow (degrees 0 to 3) in patients with AMI treated with thrombolytic therapy. Four hundred twenty-two patients (median age 57 years, 355 men) with AMI were treated with intravenous streptokinase and followed prospectively for up to 8 years. At the end of the study period, patients with collateral coronary flow 3 (n = 30) and those with flow <3 (n = 392) at in-hospital coronary arteriography had survival rates of 66% and 85%, respectively (p <0.12). Meanwhile, patients with coronary anterograde flow 3 (n = 189) and those with flow <3 (n = 233) had survival rates of 89% and 80%, respectively (p <0.04). By censored regression analysis, a negative correlation was found between coronary collateral flow degree and survival (p = 0.0498) and, inversely, a positive correlation was found between coronary anterograde flow degree and survival (p = 0.0053). By Cox multivariate analysis, the following variables showed significant correlations with long-term survival: global left ventricular ejection fraction (p = 0.0003), anterograde flow degree (p = 0.0006), collateral flow degree (negative correlation, p = 0.0179), and medical treatment (negative correlation, p = 0.0464). Thus, patients treated with intravenous streptokinase during AMI and with adequate coronary collateral circulation had a worse prognosis than those who developed adequate anterograde flow, probably because of residual myocardial ischemia. Such patients may benefit from coronary revascularization (angioplasty or surgery) to restore anterograde blood flow and minimize myocardium at risk.

Effect of niacin and etofibrate association on subjects with coronary artery disease and serum high-density lipoprotein cholesterol <35 mg/dl.

Niacin treatment (alone) was compared with etofibrate and niacin combination to treat patients with high-density lipoprotein <35 mg/dl and without hypertriglyceridemia. The niacin and etofibrate combination proved to be safe and increased high-density lipoprotein cholesterol levels to 48%, which was 3 times higher than that obtained with niacin alone.

Coronary angioplasty results in leukocyte and platelet activation with adhesion molecule expression. Evidence of inflammatory responses in coronary angioplasty.

OBJECTIVES: This study sought to characterize leukocyte and platelet activation and adhesion molecule expression after coronary angioplasty. BACKGROUND: Coronary angioplasty can be regarded as a clinical model of postischemic inflammation because this intervention leads to the release of inflammatory mediators as a result of plaque rupture and endothelial injury. METHODS: In 13 patients with stable angina (mean [ +/- SEM] age 56.0 +/- 2.4 years, range 44 to 79), blood samples were drawn from the aorta and coronary sinus immediately before and immediately and 15 min after coronary angioplasty. Subsequently, leukocyte and platelet functions were determined. Eleven control patients (57.5 +/- 2.3 years, range 52 to 78) underwent coronary arteriography. RESULTS: Coronary arteriography and angioplasty showed no difference in number of leukocytes between the coronary sinus and the aorta. However, 15 min after coronary angioplasty, there was an increase in neutrophil CD18 and CD11b, monocyte CD14 and platelet glycoprotein IIb/IIIa expression and a decrease in neutrophil L-selectin expression (189 +/- 25%, 163 +/- 27%, 158 +/- 35%, 141 +/- 22% and 31 +/- 10%, respectively, p < 0.01). In the control subjects, no change in adhesion molecule expression occurred. Superoxide production and aggregation in ex vivo-stimulated neutrophils collected from the coronary sinus 15 min after coronary angioplasty was significantly decreased compared with that after coronary arteriography (54 +/- 12% vs. 106 +/- 30% and 58 +/- 11% vs. 102 +/- 29%, respectively, p < 0.01). The reduced responses to phorbol ester stimulation may be explained by previous in vivo activation of neutrophils during coronary angioplasty. CONCLUSIONS: Coronary angioplasty increases neutrophil, monocyte and platelet adhesion molecule expression and induces a significant decrease in ex vivo-stimulated neutrophil superoxide generation and aggregation. These findings suggest that coronary angioplasty triggers cellular activation with an inflammatory response that could contribute to restenosis.

pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression.

Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 h decreased ICAM-1 to 60.6 +/- 9.7% of control. In contrast, alkalosis with 0% CO2 for 4 h enhanced ICAM-1 expression to 143.8 +/- 10.1% of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-alpha (TNF-alpha; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5% CO2-, TNF-alpha-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 +/- 7.8% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CD18-mediated neutrophil adhesion despite a decrease in ICAM-1 expression.

Superoxide and hydrogen peroxide induce CD18-mediated adhesion in the postischemic heart.

A burst of endothelial derived oxidants including hydrogen peroxide (H2O2) and superoxide (.O2-) occurs on reperfusion of ischemic tissues that directly causes injury; however, it is not known if this also triggers further injury due to subsequent leukocyte adhesion and adhesion molecule expression. Therefore, studies were performed in an isolated heart model developed to enable study of the role of isolated cellular and humoral factors in the mechanism of postischemic injury. Isolated rat hearts were subjected to 20 min of 37 degrees C-global ischemia followed by reperfusion with polymorphonuclear leukocytes (PMNs) and plasma in the presence or absence of superoxide dismutase (SOD), 200 U/ml, or catalase, 500 U/ml. Measurements of contractile function, coronary flow, high-energy phosphates, free radical generation, and PMN accumulation were performed. Adhesion molecule expression was measured on the surface of effluent PMNs by fluorescence flow cytometry and within the tissue using immunohistochemistry. SOD or catalase treatment resulted in 2- to 3-fold higher recoveries of contractile function, coronary flow, and high energy phosphates. EPR spin trapping measurements demonstrated that SOD totally quenched the free radical generation observed upon reperfusion while catalase prevented the formation of hydroxyl and alkyl radicals derived from superoxide. SOD or catalase treatment decreased PMN accumulation in the reperfused heart and prevented the marked upregulation of CD18 expression seen after reperfusion. These experiments demonstrate that in addition to their direct antioxidative actions, SOD and catalase each decrease PMN adhesion and CD18 expression resulting in marked suppression of PMN-mediated injury in the postischemic heart. Thus, endothelial derived H2O2 and .O2- further amplify postischemic injury by triggering CD18 expression on the surface of PMNs leading to increased PMN adhesion within the heart.

Prognostic significance of ST-T segment alterations in patients with non-Q wave myocardial infarction.

OBJECTIVE: To determine whether, among patients with non-Q wave myocardial infarction, the characteristics of the segment ST-T shifts at presentation in the diagnostic electrocardiogram can identify those with more severe coronary artery disease and predict a poor clinical outcome. DESIGN: Prospective controlled clinical trial. SETTING: Primary referral medical centre. PATIENTS: 93 patients (mean (SD) 62.0 (7.5) years) were studied: 41 with non-Q wave myocardial infarction and T wave inversion and 52 with ST segment depression. Cardiac events and mortality rates were assessed over 42 months. Age, sex, risk factors, creatinine kinase MB isoenzyme peak, and left ventricular function were comparable. RESULTS: 31 patients with T wave inversion myocardial infarction (94.6%) had total occlusion of the infarct related artery, compared with 12 patients with ST segment depression myocardial infarction (26.7%) (P < 0.05). When compared with patients with T wave inversion, patients with ST segment depression had a higher incidence of cardiac events during the first month and in the 41 subsequent months: 9.6% and 30.8% v 0% (P < 0.01) and 9.8% (P < 0.02), respectively. For the same observation periods, the mortality rates in patients with T wave inversion were 4.9% and 7.3%, and in patients with ST segment depression they were 5.8% and 9.6%, respectively. CONCLUSION: These data suggest that during a non-Q wave myocardial infarction the presence of ST segment depression is related to higher rates of short and long term cardiac events when compared with T wave inversion--possibly because of a higher incidence of residual stenosis of the infarct related artery.

Hydrogen peroxide and superoxide modulate leukocyte adhesion molecule expression and leukocyte endothelial adhesion.

While endothelial oxidant generation and subsequent leukocyte chemotaxis and activation are important mechanisms of tissue damage in ischemic organs, it is not known if oxidant generation may be involved in triggering the subsequent leukocyte-mediated injury which occurs. Questions remain whether particular oxidants and oxygen-free radicals are capable of modulating the expression of leukocyte adhesion molecules and effecting leukocyte endothelial adhesion. Studies were performed to determine the effect of different biologically occurring oxidant molecules and oxygen free radicals including: .O2-, .OH, and H2O2 on the expression of integrin and selectin adhesion molecules on the surface of human PMNs and to determine the effect of these alterations on PMN adhesion to the endothelium. Adhesion molecule expression on the surface of human PMNs was measured by immunofluorescence flow cytometry. Electron paramagnetic resonance spectroscopy was applied to characterize the presence of exogenous free radical generation as well as that from activated PMNs. It was observed that these oxidants can cause up-regulation of CD11b and CD18 expression with shedding of L-selectin. The kinetics and dose-response of these effects were analyzed and their functional significance determined by measuring PMN adhesion to cultured human aortic endothelial monolayers. These studies demonstrate that oxygen free radicals and non-radical oxidants can directly trigger PMN activation and adhesion to vascular endothelium.

Importance of the time of onset of supraventricular tachyarrhythmias on prognosis of patients with acute myocardial infarction.

It is known that left ventricular (LV) function, severity of coronary artery disease, and the presence of ventricular arrhythmias are major determinants of prognosis in patients surviving an acute myocardial infarction (AMI). However, little is known about the relationship between the time of onset of supraventricular tachyarrhythmias (SVTs) and mortality. Therefore, this study was carried out in a 48-months period on 131 patients with AMI who presented with SVT during hospitalization. Of these, 53 patients (40.5%) had arrhythmia within < 12 h of MI, while 78 patients (59.5%) had arrhythmia between 12 h and 4 days. The arrhythmias studied were atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia. The patients were similar for age, gender, coronary risk factors, creatine kinase-MB peak, cardioversion and LV function. Angiographic features for patients with the < 12-h onset of arrhythmia were: 86.7% of the patients had uniarterial lesions, 8.9% had biarterial lesions, and 4.4% had triarterial lesions. Patients with the 12-h-4-day onset had 16.1%, 53.2%, and 30.6% (p < or = 0.05) of the respective lesions. Inferior wall myocardial infarction was more frequent among patients with the earlier onset (60.4%), while patients with the later onset presented more anterior wall infarctions (50.0%). Only 11.3% of the patients with the earlier onset presented with severe in-hospital congestive heart failure (Killip classes III-IV), versus 62.8% of the patients with the later onset (p < or = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

[Acute atrial fibrillation in the emergency room. Which is the best drug for a rapid sinus rhythm conversion?]. / Fibrilação atrial aguda na unidade de emergência. Qual a droga ideal para rápida reversão ao ritmo sinusal?

PURPOSE: To evaluate differences between amiodarone, procainamide and quinidine in the time delay necessary to convert acute atrial fibrillation (AF) to sinus rhythm. METHODS: Sixty patients with acute AF were randomized in three groups (G) and treated with: quinidine (QG)-(21 patients) i.v. digital + quinidine up to 600 mg; procainamide (PG)-(23 patients) i.v. digital + i.v. procainamide, 10 mg/kg; amiodarone (AG)-(16 patients) i.v. amiodarone, 5 mg/kg. To evaluate time delay to conversion, all patients have their rhythm recorded by Holter system during four hours. Statistics were done with x2, considering significant a p < 0.05. RESULTS: There were no differences between groups regarding to age, gender and delay from symptoms initiation and medical assistance. Conversion to sinus rhythm occurred, in QG-71.4% cases; PG-47.8% and AG-50% (p > 0.05). Time delay in minutes to conversion were, respectively (media +/- SD): QG-112 +/- 43; PG-44.1 +/- 28; AG-20 +/- 13, significantly lower in PG and AG related to QG (p = 0.001). Although not significant, side effects were observed mostly in PG. CONCLUSION: Amiodarone is a good choice to convert, very quickly, acute AF. Otherwise, quinidine has the best rate of conversion but with a longer time delay.

Cardioprotective actions of a monoclonal antibody against CD-18 in myocardial ischemia-reperfusion injury.

BACKGROUND: Previous studies have demonstrated that polymorphonuclear leukocytes (PMNs) are locally activated in reperfused myocardium and contribute to the myocardial cell injury associated with reperfusion. It has been suggested that the adhesion of activated PMNs in reperfused myocardium is mediated by the PMN adhesion molecule CD-18. In the present study, we performed experiments to determine if the specific anti-CD-18 monoclonal antibody (MAb) R15.7 can prevent PMN adhesion and PMN-mediated reperfusion injury in the heart. METHODS AND RESULTS: Studies were performed with isolated, Langendorff-perfused rat hearts (nine per group) in which the hearts were subjected to 20 minutes of global ischemia followed by 45 minutes of reperfusion. Human PMNs (50 million) and rat plasma (HNRP) were infused directly into the coronary circulation of nonischemic and postischemic hearts. When HNRP was administered to nonischemic hearts, no significant alterations in coronary flow, left ventricular developed pressure, or left ventricular end-diastolic pressure were observed. When hearts were reperfused in the presence of HNRP, however, marked impairment of contractile function was observed with more than 90% reduction in coronary flow throughout the reperfusion period (P < .001 versus baseline). In addition, left ventricular developed pressure was significantly depressed (P < .001 versus baseline) throughout the reperfusion period in the HNRP group and recovered to only 13.0 +/- 3.0% at 45 minutes of reperfusion. Moreover, left ventricular end-diastolic pressure was significantly elevated (P < .001) in the HNRP group throughout the reperfusion period. Treatment with the anti-CD-18 monoclonal antibody MAb R15.7 (20 micrograms/mL) at the time of reperfusion resulted in a 92.9 +/- 4.9% recovery of coronary flow (P < .001 versus HNRP) as well as a 71.0 +/- 10.1% recovery of left ventricular developed pressure (P < .001 versus HNRP). Administration of MAb R15.7 also very significantly attenuated the elevation in left ventricular end-diastolic pressure that was observed in the untreated HNRP (30.2 +/- 7.8 versus 110.3 +/- 10.3 mm Hg, P < .001) at 45 minutes of reperfusion. Cardiac myeloperoxidase activity, an index of PMN accumulation, was markedly reduced in the MAb R15.7 group at 45 minutes of reperfusion compared with the HNRP group (0.03 +/- 0.01 versus 0.3 +/- 0.05, P < .001). To determine that the protective effect of MAb R15.7 was based on functional blocking of CD-18, additional experiments were performed with identical concentrations of MAb 3.1, which binds to the alpha-subunit of LFA-1. This PMN-binding but non-CD-18-blocking antibody had little effect on the recovery of postischemic function or coronary flow and did not reduce tissue myeloperoxidase activity. CONCLUSIONS: The administration of a specific anti-CD-18 monoclonal antibody, MAb R15.7, attenuates much of the PMN-mediated contractile dysfunction associated with this in vitro model of myocardial ischemia-reperfusion injury by limiting PMN accumulation. We conclude that CD-18-mediated adhesion may play a critical role in the pathogenesis of PMN-induced myocardial injury.

Acute myocardial infarction after simultaneous thrombosis in normal right and left coronary arteries.

A 32-year-old male patient with clinical and electrocardiographic evidence of acute myocardial infarction underwent coronary angiographic study. We observed nonocclusive thrombosis simultaneously in right and left anterior descending coronary arteries, without confirmation of spasm or obstructive artery disease in other coronary branches. Documentation of coronary thrombosis in more than one artery is rare, and its pathophysiology is still unknown. With the advent of thrombolytic therapy and immediate coronary angiographic studies in patients with evolving myocardial infarction, it has been possible to confirm the presence of thrombus and the type of coronary disease. In this case, we observed total lysis of both thrombi and the final aspect of "normal" angiographically reperfused coronary arteries.

[Use of intravenous hydralazine in treatment of hypertensive crisis]. / Uso da hidralazina intravenosa para o tratamento da crise hipertensiva.

PURPOSE: To evaluate the efficacy and safety of intravenous hydralazine in arterial hypertension. PATIENTS AND METHODS: 12 patients, mean age 45.33 +/- 15.82.8 men and 4 women all of them with systolic (S) arterial pressure (AP) greater than or equal to 180 and or diastolic (D) greater than or equal to 126 mmHg with symptoms like headache, in characteristic thoracic pain and others but without an hypertensive emergency neither acute manifestation of hypertensive encephalopathy through fundi examination were studied. The AP was taken 10 minutes after rest (initial) and 5, 15, 30 and 60 min (final) after intravenous administration of hydralazine-HCL (5 mg) which was repeated when at least 20% AP reduction was not achieved. RESULTS: The initial and final SAP, DAP and heart rate (HR) were 208 +/- 19.4 and 176 +/- 17.2 (p less than 0.0001), 133 +/- 11.3 and 112 +/- 11.5 (p less than 0.001) and 72 +/- 12.9 and 80 +/- 15.5 (NS), respectively. Side effects related to the drug were observed in 3 (25%) patients. One had symptomatic orthostatic hypotension, the second had precordial pain with ST-T changes compatible with myocardial ischemia and the third presented a thorax and abdominal cutaneous erythema, but all of them reversible. CONCLUSION: Intravenous hydralazine-HC1 is an alternative when rapid arterial pressure reduction is needed.