Biomedical subjects
Publications and source records attributed to J Lopez-Sendon.
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BACKGROUND: Although intravenous glycoprotein IIb/IIIa inhibitors are beneficial in patients with acute coronary syndromes, prolonged oral IIb/IIIa inhibition might provide an additional reduction in recurrent events. METHODS AND RESULTS: Investigators at 888 hospitals in 29 countries enrolled 10 288 patients with acute coronary syndromes, which was defined as ischemic pain at rest within 72 hours of randomization, associated with positive cardiac markers, electrocardiographic changes, or prior cardiovascular disease. Patients received aspirin and were randomized to receive, for the duration of the trial, (1) 50 mg of orbofiban twice daily (50/50 group), (2) 50 mg of orbofiban twice daily for 30 days followed by 30 mg of orbofiban twice daily (50/30 group), or (3) a placebo. The primary composite end point was death, myocardial infarction, recurrent ischemia requiring rehospitalization, urgent revascularization, or stroke. The trial was terminated prematurely because of an unexpected increase in 30-day mortality in the 50/30 orbofiban group. Mortality through 10 months was 3.7% for the placebo group versus 5.1% in the 50/30 group (P=0.008) and 4.5% in the 50/50 group (P=0.11). There were no differences in the primary end point (22.9%, 23.1%, and 22.8%, for the placebo, 50/30, and 50/50 groups, respectively). Major or severe bleeding (but not intracranial hemorrhage) was higher with orbofiban; it occurred in 2. 0%, 3.7% (P=0.0004), and 4.5% (P<0.0001) of patients, respectively. Exploratory subgroup analyses found that patients who underwent percutaneous coronary intervention had a lower mortality and a significant reduction in the composite end point (P=0.001) with orbofiban. CONCLUSIONS: -Fixed-dose orbofiban failed to reduce major cardiovascular events and was associated with increased mortality in this broad population of patients with acute coronary syndromes; however, a benefit was observed among patients who underwent percutaneous coronary intervention.
Patients with acute myocardial infarction (MI) and cardiogenic shock constitute a very high risk subset despite an aggressive management. The objective of this study was to evaluate if the results of early coronary angioplasty in patients with acute myocardial infarction and cardiogenic shock have changed over the last years, and to address which role the recent adjuvant therapies have played in this evolution. From 1991 to April 1999, 94 patients with acute MI and cardiogenic shock were treated with coronary angioplasty within the first 12 hours from the onset of symptoms. Temporal changes of the utilization of adjuvant therapies and operators experience were studied over these years, as well as their impact on the angiographic results and in-hospital outcome. Over the years, a progressive and significant increase on the use of coronary stents and c7E3Fab was observed, as well as an increased number of primary angioplasties performed per month. The proportion of patients treated with intraaortic balloon pump did not changed significantly over the years. An angiographic successful result (< 50% residual stenosis and TIMI flow 2 or 3) and a final TIMI grade 3 flow were obtained in 76 (80.9%) and 61 (64.9%) patients, respectively. The angiographic success rate progressively increased over the years, from 72.3% in patients treated before 1994 to 94.1% in those admitted in 1998Eth 1999 (p for trend 0.0409). The proportion of patients with a final TIMI grade 3 flow also grew progressively over the years: from 36.4% before 1994 to 76.5% after 1997 (p for trend 0. 0209). The overall in-hospital mortality rate was 63.8% (60 patients), and there was no significant change in mortality rate over the years. Therefore, apart from the growing operators experience, we have observed an incremental change in the use of coronary stents and c7E3 Fab (abciximab) in patients with acute myocardial infarction and cardiogenic shock treated with early coronary angioplasty. All these factors have led to an improvement in the angiographic results, although this change has not meant a significant reduction of mortality.
Isolated right ventricular infarction has been found in cases of right ventricular hypertrophy, but there are no reports on right ventricular infarction secondary to massive pulmonary embolism. Six autopsied patients with massive pulmonary embolism and pure right ventricular infarction, suspected to be secondary to the embolism, were selected from a population of 216 autopsies. Pulmonary embolism was the suspected diagnosis in five cases due to typical clinical, electrocardiographic and haemodynamic data. Right ventricular infarction was a post-mortem finding, not previously diagnosed. In every case the thickness of the right ventricular myocardium was normal. The necrosis of the right ventricle was transmural in four cases and subendocardial in two and the entire right ventricular wall (anterolateral as well as posterior) was involved. No mural thrombi were present and in no case did the necrosis involve the left ventricle. In one case the coronary arteries were normal, in the other five significant lesions of the right or left coronary arteries were observed. These lesions may have been, in part, responsible for the necrosis of the right ventricle when the massive pulmonary embolism was added. We conclude that right ventricular infarction may be secondary to pulmonary hypertension in the setting of massive pulmonary embolism, even in the absence of right ventricular hypertrophy and with normal or stenotic coronary arteries.
Acute ischaemia limited to the free wall of the right ventricle was produced by right coronary arterial ligation (RCAL) in 20 dogs. Contrast M-mode and cross-sectional echocardiography was performed in 7 cases to investigate the presence of tricuspid insufficiency. The haemodynamic findings obtained with an open pericardium at 15 to 30 min showed increases in right (1.2 +/- 0.5 to 2.7 +/- 0.7 mmHg, P less than 0.01) and left (5.0 +/- 0.8 to 6.6 +/- 0.9 mmHg, P less than 0.05) ventricular end-diastolic pressures, and decreases in heart rate (139 +/- 4.9 to 119 +/- 5.1 bpm, P less than 0.01), cardiac index (106 +/- 6.6 to 81 +/- 7.3 ml min-1 kg-1, P less than 0.01), stroke index (79 +/- 6 to 72 +/- 8 ml X 100 beat-1 kg-1, P less than 0.02), right (23.8 +/- 1.5 to 19.4 +/- 1.5 mmHg, P less than 0.01) and left (109 +/- 7.2 to 95 +/- 8.2 mmHg, P less than 0.05) ventricular systolic pressures and right ventricular stroke work index (18.3 +/- 2.4 to 11.4 +/- 1.8 g m kg-1, P less than 0.01). In 6 of 15 cases the 'y' descent became deeper than the 'x' descent in right atrial pressure (RAP). Tricuspid insufficiency grade I-II/IV was present in 3 of 7 cases, 2 of them with a 'y' greater than 'x' in RAP. Right ventricular mechanical alternans, probably secondary to a decrease in contractility, appeared in 10 of 20 cases after RCAL.(ABSTRACT TRUNCATED AT 250 WORDS)
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To determine the sensitivity, specificity, predictive value and diagnostic efficiency of electrocardiographic alterations in the diagnosis of acute right ventricular infarction, 43 autopsy patients with acute myocardial infarction and an electrocardiogram including 12 leads plus leads V3R and V4R were studied. Group A included 21 patients with right ventricular infarction, of whom 14 (group AI) had posterior and 7 (group AII) had anterior right ventricular infarction. Group B included 22 patients without right ventricular infarction. Excluding group AII patients, the sensitivity of the presence of a Q wave reached 78.6% in lead V4R and decreased in leads V1 to V3; its specificity was low in all the leads. The sensitivity of ST segment elevation reached 100% in lead V4R and decreased in leads V1 to V3; its specificity was highest (68.2%) in leads V4R and V3R, its negative predictive value was 100% and its diagnostic efficiency was 80.6%. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 was less sensitive (78.6%) than ST segment elevation in lead V4R alone, but its specificity reached 100%, its positive predictive value 100% and its diagnostic efficiency 91.7%. In conclusion, there are no electrocardiographic criteria to identify anterior right ventricular necrosis, but posterior right ventricular necrosis may be identified by the presence of a Q wave or ST segment elevation in the right precordial leads, reaching the highest sensitivity and specificity in lead V4R. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 offers the highest specificity and efficiency in the diagnosis.
The echocardiographic characteristics of hemopericardium with and without thrombus formation were investigated in 10 dogs and compared with that of saline solution injected into the pericardial cavity. Injection of 80 to 120 ml of saline solution produced an echolucent space between both pericardial layers and was considered as the control image in each dog for comparison with hemopericardium. Injection of heparinized blood filled the pericardial cavity with irregular echoes of variable acoustical impedence. High-density echoes of irregular distribution were observed in 3 dogs, in 5 dogs the echoes were of low acoustical density and in 2 dogs blood echoes were present but scarcely visible. Injection of clotted blood in 9 dogs (adding 20 mg of protamin sulphate and 8 mg of aminocaproic acid) produced echoes of high acoustical density easily identified in the 2-dimensional echocardiographic images. In 4 dogs attenuation and damping controls were increased to the point where myocardial echoes disappeared, while intrapericardial echoes were still visible. Thus, hemopericardium with or without thrombus formation may be identified by 2-dimensional echocardiography and differentiated from other types of pericardial effusion of lower acoustical density. Echogenicity of fluid blood in the pericardial cavity may be related to blood stasis.
Eleven patients with cardiogenic shock following acute myocardial infarction (AMI) have been treated with prenalterol. This drug was administered in seven patients once dobutamine or dopamine proved to be ineffective or poorly effective, and it was the first inotropic drug employed in four patients. Therapeutic dose of intravenous infusion ranged from 2.2 to 18 micrograms/kg/min (mean dose: 7 micrograms/kg/min), and was maintained for 2 to 4 hours. Since two patients received the infusion on two different occasions, a total of 13 cases were considered for statistical analysis. Prenalterol produced an increase in cardiac index (p less than 0.01), mean aortic pressure (p less than 0.02), net work index (p less than 0.01), net/stroke work index (p less than 0.01), pressure rate product (p less than 0.05), and myocardial perfusion gradient (p less than 0.02). It decreased systemic (p less than 0.02) and pulmonary (p less than 0.01) vascular resistances, pulmonary artery (p less than 0.01) and pulmonary capillary (p less than 0.05) pressures. Heart rate and right atrial pressure were not significantly changed. The drug acted as a relatively selective inotropic agent without a chronotropic effect and with minimal peripheral actions. It was effective in seven patients and ineffective in four patients. Thus prenalterol appears to be a useful drug in cardiogenic shock and further studies are warranted.
Six patients with subacute left ventricular free wall rupture (anatomically proved) following acute myocardial infarction are presented. Diagnosis of cardiac rupture in every case was suspected several hours before death or surgical intervention, when clinical and hemodynamic data of cardiac tamponade were found. In three patients right atrial pressure decreased with inspiration and in the other three cases it did not show any modification. These latter three patients had associated right ventricular infarction; the abnormal respiratory behavior could be explained by restriction produced by a noncompliant right ventricle. All six patients improved initially with medical treatment (inotropics and fluid infusion) and three of them were operated upon. One of the latter patients died on the eighteenth postoperative day of extracardiac causes and two are long-term survivors.
Right ventricular (RV) segmental contraction was studied in 63 patients with acute myocardial infarction (MI), using 2-dimensional (2-D) echocardiography. Group A included 32 patients with ischemic RV dysfunction: 19 had a disproportionate increase in right atrial pressure at the time of the examination (Group AI) and in 13 patients, right atrial pressure was normal when the echocardiogram was obtained (Group AII). Group B included 31 patients without ischemic RV dysfunction. Alkinesia or dyskinesia of the RV wall was found in 30 patients: 19 from Group AI, 8 from Group AII, and 3 from Group B. Asynergy could be identified in all segments of the RV wall including the outflow tract, RV apex, and anterior wall, but was more frequently found in the posterior wall (29 patients), best seen in the transversal subcostal short-axis view. A significant difference was found either in the frequency of wall motion abnormalities or in the number of segments with asynergy among the 3 groups (p less than 0.001). However, asynergy of the RV wall may be present in some patients with normal right heart hemodynamic function, suggesting that asynergy may be more sensitive than hemodynamic function in the diagnosis of acute RV infarction. Paradoxical septal motion was found in 8 patients, all in Group AI, and all had a right atrial pressure equal to or greater than pulmonary capillary pressure.
The haemodynamic effect of several vasodilators was studied in 15 patients with pulmonary hypertension of recent onset secondary to ingestion of toxic oil. Right heart catheterization was performed by means of a Swan-Ganz thermodilution catheter. Mean pulmonary artery pressure (PAP) was higher than 25 mmHg in every patient. Haemodynamic monitoring was maintained for 2-3 days and three drugs were administered. Nifedipine (10 mg sublingual plus 20 mg p.o.) produced slight reductions in PAP and pulmonary artery resistance (PAR) at some time after drug administration. These changes were minimal and the drug was not considered useful. Nitroglycerine ointment (20-25 mg) produced a significant decline in PAP and PAR throughout six hours although prominent changes occurred only at the first hour. Prazosin (5-10 mg p.o.) induced a significant decline in PAR and PAP throughout 6 hours. The effect of this drug was more prominent than that of nitroglycerine.
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To test the sensitivity and specificity of hemodynamic criteria for acute right ventricular infarction (RVI), two groups of patients with anatomically proved acute myocardial infarction and hemodynamic monitoring were studied. Group A included 22 patients acute RVI and group B, 38 with infarction confined to the left ventricle. In both groups, the closest relation between right atrial and pulmonary capillary pressures (RAP and PCP), as well as the presence of a severe noncompliant pattern (SNCP), were studied. A SNCP was defined as a y descent deeper than the x descent in RAP. RAP was equal to or higher than PCP in 10 patients from group A and in none from group B. In group B, a significant relation was found between RAP and PCP (r = 0.777, y = 0.43x + 0.18) (p less than 0.05), and the 95% confidence limits could be calculated. Above these limits, a closer relation between RAP and PCP was only found in patients with RVI. However, six patients with RVI showed an RAP/PCP relation within 95% confidence limits of group B (sensitivity 72.7%, specificity 100%). A SNCP was present in 12 patients with RVI and only in one without RVI (p less than 0.01) (sensitivity 54.5% and specificity 97.4%). When either criterion is present (close relation between RAP and PCP or SNCP), a high sensitivity (81.8%) and specificity (97.4%) can be achieved in the diagnosis of acute RVI.
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Ischemic right ventricular dysfunction was diagnosed in 54 patients with acute myocardial infarction who had a right atrial pressure disproportionately increased in relation to the pulmonary capillary pressure. The right atrial pressure curve in 40 patients (74 percent) was M- or W-shaped, termed a noncompliant pattern, and was similar to the pattern found in constrictive pericarditis. Kussmaul's sign was found in the patients whose respiration was recorded. This pattern, which represents poor right ventricular compliance, was severe in 30 cases (y descent greater than x descent) and slight in 10 cases (y descent = x descent). Its duration was variable, ranging from days to years. Of the 54 patients, 32 (59 percent) had a low output syndrome, diagnosed in the presence of a cardiac index of less than 2.2 liters/min per m2, with signs of poor tissue perfusion. The severe noncompliant pattern was significantly related to the presence of a low output syndrome (p less than 0.01) and mortality from this cause (p less than 0.05). The jugular venous tracing pulse had a pattern similar to that of the right atrial pressure recording and therefore may be valuable in the noninvasive diagnosis of right ventricular dysfunction and in the study of the evolution of the noncompliant pattern and, hence, of ventricular compliance.
In this paper we describe clinical and hemodynamic data in ten patients with right ventricular infarction and low output syndrome. Atrioventricular block and supraventricular arrhythmias were a common finding. All of them had a right atrial pressure disproportionately increased (average 16.3 +/- 5.2 mm. Hg) in relation to left ventricular filling pressure (average 15 +/- 4.5 mm. Hg), and a very low cardiac index (average 1.42 +/- 0.45 liters/min./m.2). The right atrial pulse tracings were similar to those of constrictive pericarditis, showing a deep "y" descent in every patient. We made the differential diagnosis between similar hemodynamic entities and constructed function curves of right and left ventricles. Right ventricular diastolic work index was always increased (average 6.26 +/- 3.63 gm./beat/M.2), being higher than net work index (average 3.28 +/- 1.87 gm./beat/M.2). While all function curves of the right ventricle were flat or depressed, those of the left ventricle were very different. Treatment consisted mainly of fluid overload and, in some cases, of vasodilators or dopamine. Mortality rate was 40%. We think that coexisting left ventricular damage may account in part for the bad prognosis of these patients.