Effect of coronary artery recanalization on right ventricular function in patients with acute myocardial infarction.

The effects of coronary artery recanalization by intracoronary administration of streptokinase on left ventricular function during acute myocardial infarction have received increasing attention in recent years. Although myocardial dysfunction is often more pronounced in the right ventricle than in the left ventricle in patients with acute inferior wall myocardial infarction, the effect of coronary artery recanalization on right ventricular dysfunction has not been previously addressed. Accordingly, in this investigation, 54 patients who participated in a prospective, controlled, randomized trial of recanalization during acute myocardial infarction were studied. Among 30 patients with inferior wall infarction, 19 had right ventricular dysfunction on admission; 11 of these 19 had positive uptake of technetium-99m pyrophosphate in the right ventricle, indicative of right ventricular infarction. Patients with successful recanalization (n = 6) exhibited improved right ventricular ejection fraction from admission to day 10 (26 +/- 7 to 39 +/- 14%, p less than 0.03). However, control patients (n = 6) and patients who did not undergo recanalization (n = 7) also exhibited improvement (20 +/- 7 to 29 +/- 11% [p less than 0.02] and 30 +/- 8 to 40 +/- 6% [p less than 0.03], respectively). Improvement in several other variables of right ventricular dysfunction evolved at an equal rate with the ejection fraction changes. Patients with or without right ventricular infarction improved similarly. These data indicate that the right ventricular dysfunction commonly associated with inferior wall infarction is often transient, and improvement is the rule, irrespective of early recanalization of the "infarct vessel."

Sustained ventricular tachycardia in chronic chagasic myocarditis: electrophysiologic and pharmacologic characteristics.

Sustained ventricular tachycardia (VT) develops in many patients with chronic Chagasic myocarditis. Programmed stimulation was used to study the electrophysiologic characteristics of VT in 15 patients with Chagas' cardiomyopathy. Nine patients were in New York Heart Association functional class I, 5 were in class II and 1 patient was in class III. The average ejection fraction was 56 +/- 7%, which is somewhat better than that reported in patients with VT owing to idiopathic cardiomyopathy. In 11 patients VT could be reproducibly initiated and terminated by programmed stimulation. Intravenous mexilitene prevented induction of VT in 7 of 8 patients; amiodarone did not prevent induction in 3 of 4 patients. Our data indicate that the mechanism of VT is likely to be reentrant in many patients, and therefore VT can be produced by extrastimuli. Electrophysiologic study is therefore useful for establishing the diagnosis of sustained VT and may be useful for guiding initial therapy in selected cases of Chagas' disease.

Intracoronary thrombolytic therapy in acute myocardial infarction: a prospective, randomized, controlled trial.

A prospective, randomized trial was designed to assess the efficacy of intracoronary thrombolytic therapy with streptokinase (STK) in acute myocardial infarction. Sixty-four patients with acute myocardial infarction were randomized within 6 hours of onset of symptoms to 1 of 3 groups. Sixteen patients were treated by conventional means (control group). Nineteen patients underwent coronary arteriography and received corticosteroids and intracoronary and intravenous nitroglycerin (NTG group). Twenty-nine patients received management identical to that of the NTG group, with the addition of intracoronary STK therapy (STK group). Recanalization was demonstrated in 21 of 29 patients (72%) in the STK group. Global and regional ejection fraction (EF) was determined by radionuclide ventriculography before any intervention and 7 to 10 days later. No significant improvement in global EF was achieved in the control and NTG groups. In STK patients as a group, global EF did not increase significantly; however, in patients recanalized with STK, EF improved from 42 +/- 17% to 49 +/- 16% (p = 0.023). All groups showed wide variability of response. Improvement in global EF of more than 5% was noted in 44% of patients recanalized with STK. When subgrouped on the basis of initial global EF of 45% or less or more than 45%, only patients recanalized with STK with an initial EF of 45% or less had an improved global EF (from 30 +/- 10% to 42 +/- 10%, p = 0.015).(ABSTRACT TRUNCATED AT 250 WORDS)

The cardiovascular effects of acute hypoxemia as a diagnostic aid.

Acute hypoxemia produces opposite effects on the pulmonary and systemic vascular resistance. To assess the influence of acute hypoxemia on cardiac murmurs, 36 patients with a single valvular or congenital heart lesion were studied. As expected from these hemodynamic effects, right-sided regurgitant type murmurs increased in intensity during acute hypoxemia, while stenotic type murmurs were reduced. In contrast, left-sided murmurs remained constant or changed in opposite direction to their equivalent type from the right side. Additionally, acute hypoxemia produced a marked reduction of the murmurs due to left-to-right shunts and allowed an adequate differentiation of the murmurs due to ventricular septal defect from those due to mitral incompetence.

Rapid attenuation of response to nifedipine in primary pulmonary hypertension.

In a 22-year-old woman with primary pulmonary hypertension resistant to all previous attempts to reduce the pulmonary vascular resistance, there was dramatic improvement after the first dose of nifedipine, 20 mg po, which was not sustained with subsequent doses. While there was a persistent reduction in systemic vascular resistance, the initial drug-related reduction in pulmonary vascular resistance was progressively attenuated with the subsequent four doses of nifedipine, 20 mg.

An accurate and simplified method to calculate angiographic left ventricular ejection fraction.

An accurate and simplified method to calculate left ventricular (LV) ejection fraction (EF0 derived from the ellipsoidal formula for LV volume calculation is described. The LV Minor axis (D) is obtained from the average of three equidistant LV diameters at end-diastole (Ded) and end-systole (Des), and the shortening fraction of D2 (% delta D2) calculated as (D2ed - D2es)/D2ed. EF is calculated as EF = [delta D2 + ([1 - delta D2] X delta L)] X 100, where delta L = the shortening fraction of the long axis. The coefficient of correlation between the EF by this method and the EF derived from measurements of LV volumes with the area-length method was 0.98, SEE = 3.57% (n = 50). No significant over- or underestimation was observed according to the regression equation Y = 0.922X + 0.82. Thus, this simplified method allows accurate LVEF calculation without the need for planimetry of LV area.

Characterization of the atherosclerotic plaque in the internal mammary artery.

The current study examines, at both structural and ultrastructural levels, representative segments of internal mammary arteries obtained from 15 male patients, ranging in age from 45 to 75 years, with signs or symptoms of coronary heart disease. These segments were obtained at the time of coronary bypass surgery. Of the 15 segments examined, only 2 were found to have atherosclerotic plaques. In other segments, only an intimal thickening similar to that observed during aging was found. There was evidence of endothelial cell loss and defects of internal elastic lamina in the present study; however, there was no evidence of lipid accumulation in the intimal region. This observation agrees with previous findings that indicate that lipid accumulation is not a necessary factor for the formation of atherosclerotic plaques. During the study microfilament bundles, the so-called "stress fibers," were also observed in the cytoplasm of the luminal side of endothelial cells. Stress fibers are known to be present in some endothelial cells in some pathologies such as regeneration after injury or hypertension. One of the features of the atherosclerotic plaques from an internal mammary artery was the presence of cells with contractile and synthetic phenotypes (contractile and synthetic smooth muscle cells), as well as cells with intermediate features. Cells with similar characteristics have also been observed during the development of the early stages of atherosclerosis, during embryological development of vessels, after experimental excimer laser treatment, and in primary cell culture. To our knowledge, this is the first report showing the ultrastructural features of the atherosclerotic plaques in the internal mammary artery.

Echocardiographic features of impaired left ventricular diastolic function in Chagas's heart disease.

To study left ventricular diastolic function in Chagas's disease, simultaneous echocardiograms, phonocardiograms, and apexcardiograms were recorded in 20 asymptomatic patients with positive Chagas's serology and no signs of heart disease (group 1), 12 with Chagas's heart disease and symptoms of ventricular arrhythmia but no heart failure (group 2), 20 normal subjects (group 3), and 12 patients with left ventricular hypertrophy (group 4). The recordings were digitised to determine left ventricular isovolumic relaxation time and the rate and duration of left ventricular cavity dimension increase and wall thinning. In groups 1 and 2 (a) aortic valve closure (A2) and mitral valve opening were significantly delayed relative to minimum dimension and were associated with prolonged isovolumic relaxation, (b) left ventricular cavity size was abnormally increased during isovolumic relaxation and abnormally reduced during isovolumic contraction, and (c) peak rate of posterior wall thinning and dimension increase were significantly reduced and duration of posterior wall thinning was significantly prolonged; both of these abnormalities occurred at the onset of diastolic filling. These abnormalities were more pronounced in group 2 and were accompanied by an increase in the height of the apexcardiogram "a" wave, an indication of pronounced atrial systole secondary to end diastolic filling impairment due to reduced left ventricular distensibility. Group 4, which had an established pattern of diastolic abnormalities, showed changes similar to those in group 2; however, the delay in aortic valve closure (A2) and in mitral valve opening and the degree of dimension change were greater in the latter group. Thus early isovolumic relaxation and left ventricular abnormalities were pronounced in the patients with Chagas's heart disease and may precede systolic compromise, which may become apparent in later stages of the disease. The digitised method is valuable in the early detection of myocardial damage.

Percutaneous mitral valve dilatation with the Multi-Track System.

We developed the Multi-Track System for percutaneous mitral valvotomy and described the preliminary results in 1995. Here we report the first 100 consecutive cases after the original publication. Two separate balloon catheters are positioned on a single guidewire. The first catheter, with only a distal guidewire lumen, is introduced into the vein and then advanced into the mitral orifice. Subsequently, a rapid exchange balloon catheter running on the same guidewire is inserted and lined up with the first catheter so the two are positioned side by side. Both balloons are then inflated simultaneously. Age of the patients was 31 +/- 12.8 years and weight 50 +/- 14 kg. Valve area increased 0.75 +/- 0.22 cm(2) to 2.00 +/- 0.32 cm(2)and mean left atrial pressure dropped from 27 +/- 8 to 11 +/- 5 mm Hg. One patient had significant mitral insufficiency after dilatation, which did not require surgery. The Multi-Track System is a valid alternative to the existing procedures for the treatment of mitral stenosis and uses simpler and less costly catheters. Cathet. Cardiovasc. Intervent. 48:178-183, 1999.

Endomyocardial disease in South America--report on 23 cases in Venezuela.

Twenty-three cases of endomyocardial disease (ED) are presented, studied in Venezuela, a tropical country in northern South America. The diagnosis was confirmed in 18 cases by means of pathological studies, and in 5 cases by angiocardiography which showed the characteristic obliterative ventricular lesions. Eosinophilia was present in 35% of the patients. The most frequent clinical feature was heart failure associated with mitral regurgitation. Systemic embolism was the first clinical feature in 5 cases. In 2 cases, ED was associated with autoimmune haemolytic anaemia or vasculitis. Necropsy revealed a predominance of the left-sided (9/16 cases) and biventricular (6/16 cases) types. The pathological lesions were characterised by fibrous thickening of the endocardium at the apex and the ventricular inflow tracts extending to the myocardium and involving the atrioventricular valves. ED is frequently misdiagnosed as rheumatic valvular cardiopathy. The two-dimensional echocardiogram is a very useful procedure for determining the spatial anatomy of ED. The echo findings were closely correlated with ventriculographic and necropsy findings. Even though ED is widely spread around the world, it is most frequently found in tropical and subtropical countries in Africa, Asia and America, such as Venezuela and Brazil. This suggests that there are aetiological factors in these latitudes, about which little is known.

Estudio sobre la miocardiopatía hipertrófica: aspectos clínicos, ecocardiográficos, hemodinámicos y angiocardiográficos en una serie de treinta pacientes / Hypertronic mycardiopathy study: clinical, ecocardiographic, ecographic, hemodynamic and angiographic aspects in series of thirty patients

Se hace la descripción clínica de la miocardiopatía hipertrófica en el medio venezolano. El estudio versó sobre los aspecto clínicos, ecocardiográficos, hemodinámicos y angiocardiográficos de esta entidad, el cual fue realizado en una serie de treinta pacientes, observados durante el lapso de 7 años (1978-1985) en nuestro país. El espectro clínico de la afección fue muy amplio, el cual abarcó desde formas asintomáticas hasta formas con sintomatología de severidad progresiva. El diagnóstico clínico se fundamentó en una historia clínica sugestiva, a veces de carácter familiar, con una signología en la que sobresalen las alteraciones del pulso, el hallazgo de un choque apexiano anormal (bífido o trífido), el latido presistólico y los soplos relacionados con la obstrucción del tracto de salida y la insufiencia valvular mitral. La enfermedad se caracterizó por un cuadro clínico de evolución progresiva. El diagnóstico clínico fue corroborado por la presencia de dos alteraciones ecocardiográficas significativas: 1) la hipertrofia septal asimétrica, 2) el movimiento sistólico anterior de la valva anterior de la válvula mitral o de ambos. En el estudio hemodinámico por la presencia de un gradiente de presión intraventricular en reposo o provocado y en la angiocardiografía por la constatación de la hipertrofia septal y de los músculos papilares. Se desconoce la prevalencia de la afección en escala mundial y nacional. Es necesario realizar estudios sobre el aspecto familiar y las alteraciones genéticas que presenta la afección en nuestro medio. Los estudios patológicos, realizados en el Instituto de Anatomía Patológica, UCV, han permitido corroborar las alteraciones estructurales características de la afección en el material patológico de nuestro medio