Biomedical subjects
Publications and source records attributed to I Coma-Canella.
The angiographic study of a young woman with previous anterior myocardial infarction and normal coronary arteries is presented. During coronary angiography the patient had multiple episodes of spasm in the right coronary artery and an acute inferior myocardial infarction.
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.
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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.
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.
The hemodynamic effects of the new oral vasocilator prazosin were evaluated in 11 patients with congestive failure following myocardial infarction. Prazosin decreased pulmonary trunk, pulmonary capillary, and right atrial pressures, systemic blood pressure, systemic vascular and total pulmonary resistances, and the heart rate X systolic blood pressure product (P less than 0.001). Cardiac and stroke indexes increased (P less than 0.001 and P less than 0.02, respectively). Heart rate, myocardial perfusion gradient, and stroke work index remained unchanged (P less than 0.05). Prazosin effect began in most patients 30 minutes after an oral administration of 2.5 to 7 mg; the maximum effect occurred from one to three hours later. The action is sustained for at least 6 hours in most patients and sometimes is present even 12 hours after a single dose administration. We conclude that prazosin, with a nitroprusside-like effect, improves left ventricular performance and myocardial O2 supply-demand relationship in patients with acute myocardial infarction, but optimal doses vary significantly, and the hazard of severe and sustained hypotension, or decline in cardiac output in patients with normal blood pressure or slightly elevated filling pressure, is present.
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BACKGROUND: Successful revascularization of ischemic asynergic myocardium should be followed by improvement in contractile function. However, a clear improvement is not always observed. Assessment of contractile reserve may allow a better evaluation of procedural results. METHODS AND RESULTS: To assess the changes in global and regional left ventricular ejection fraction (EF), as well as the contractile reserve after revascularization, equilibrium radionuclide angiography was performed in 16 patients with acute myocardial infarction who had periinfarct redistribution (observed in stress-rest-reinjection thallium single-photon emission computed tomography). Regional EF was defined in the asynergic region at rest, which corresponded to the infarct plus periinfarct areas. Both thallium single-photon emission computed tomography and equilibrium radionuclide angiography were performed at rest and during stress with dobutamine, up to a maximal dose of 40 micrograms/kg/min. The same studies were repeated 8 +/- 6 months after successful revascularization (nine coronary angioplasties and seven bypass procedures). After intervention, the thallium defect score decreased significantly at rest and during stress. Global EF changed from 45% +/- 10% to 47% +/- 11% (difference not significant) at rest and from 49% +/- 12% to 63% +/- 13% (p = 0.0001) at peak stress. Regional EF changed from 27% +/- 8% to 35% +/- 18% (p = 0.03) at rest and from 29% +/- 10% to 56% +/- 21% (p = 0.0001) at peak stress. CONCLUSIONS: In patients with asynergy caused by periinfarct ischemia, there can be an increase in regional but not global EF at rest after revascularization. However, both parameters improve at peak dobutamine dose. This indicates an improvement in contractile reserve.