[Diagnosis of myocardial ischemia by dynamic digital echocardiography with dobutamine and atropine]. / Diagnóstico de la isquemia miocárdica mediante ecocardiograma dinámico digitalizado con dobutamina y atropina.

We studied 300 patients (p) with dobutamine stress echocardiography (DSE) and atropine. The indication were chest pain, abnormal electrocardiogram (ECG), abnormal stress electrocardiogram with or without chest pain or any combination of these. The DSE was evaluated with digitized imaging in long and short parasternal views and apical four and two chambers views before and during dobutamine test with simultaneous side by side display. In 21 p (56.7%) we found positive concordance in diagnosis of coronary artery disease (CAD) between coronary arteriography (CA) and DSE. In 13 of 37 p the concordance was negative by the two methods (35.1%); then the DSE was capable correctly predict in 34 p (91%). The abnormal CA and normal DSE were found in one p (4.5%) with 90% obstruction of a small diagonal vessel. In two women DSE was abnormal with inferior hypokinesis (13.3%) and the CA was normal. In 43 p (14.3%) ECG and DSE were positive for myocardial ischemia (MI); negative concordance of both procedures was found in 203 p (67.6%). ECG was abnormal and DSE normal in 46 p (15.3%) 61 p (20.3%) with DSE abnormal in 8 p (2.6%) 61 p (20.3%) had arrhythmias; in 55 (18.3%) premature ventricular contractions, one p with ventricular tachycardia (0.33%); 7.3% of them required endovenous lidocaine. Chest pain was present in 22 p (7.3%) and the treatment waqs sublingual isosorbide; hypotension appeared in 27 p (9%) and were treated with saline infusion. Hypertensive response was found in two p (0.66%) and were treated with nifedipine and smolol. We concluded that DSE with atropine has high sensibility (95.5%) and specificity (86.6%) in the diagnosis of ischemic heart disease. The adverse effects are nondangerous and easily resolved with medical treatment.

[The mechanism of remodelling in left ventricular volume overload]. / El mecanismo de remodelación en las sobrecargas de volumen del ventrículo izquierdo.

We studied 60 people who were separated into three groups. Group A: 11 patients with pure, severe mitral regurgitation (MR); Group B: 18 patients with pure, severe aortic regurgitation (AR) [this group was divided into two: I) with normal ejection fraction (EF) and II) with low EF]. The third group was a control one with 31 healthy people. Through 2-D Echocardiography (2-D Echo) we got: diameters of the cavities, thickness of the wall, ventricular function, h/r ratio, and systolic wall stress (S). Patients with MR showed left atrial and ventricular enlargement with low h/r ratio, normal ventricular function and raised S. The group I of AR had left ventricular enlargement and hypertrophy, with normal h/r ratio and EF, and with raised S, while the group II of AR showed left ventricular enlargement, low h/r ratio and EF with very high S. In MR volumetric overload causes different anatomic and functional changes on the left ventricle than in the AR. In MR there is a systolic leak toward left atrium. This causes the low S in the beginning of the illness and is not the mechanism that trigger left ventricular hypertrophy (LVH). The absence of LVH causes excessive enlargement of the myofibril and with time there is structural damage and contractile failure which raises the systolic volume and S. Later on, hypertrophy develops. On the other hand, since the beginning AR has high S which causes adequate hypertrophy (normal h/r ratio) and later it produces huge ventricular enlargement decreases the h/r ratio (inadequate hypertrophy) with contractile failure. We conclude: the time of surgery in MR is when the patient raises S and in the AR when inadequate hypertrophy appears (low h/r) but when EF is still normal.

[Structural and functional changes in the heart of the hypertensive patient. An echocardiographic study]. / Cambios estructurales y funcionales en el corazón del hipertenso. Estudio ecocardiográfico.

We studied 15 patients with essential hypertension (EH) in whom the diagnosis was corroborated with ambulatory blood pressure monitoring (ABPM). The blood pressure levels (BP) were compared with values obtained from healthy people (HP). We studied 31 HP with 2-D echocardiogram and the parameters of ventricular performance were compared with the values obtained from EH people. ABPM shown that the EH people has higher BP values than HP around 24 hs (EH loss the circadian rhythm of BP). On the other hand the EH had left ventricular hypertrophy (LVH) with normal systolic ventricular function (VF). The systolic wall stress was low because the LVH was inappropriate. The LVH as adaptative mechanism maintains normal the VF in spite of pressure overload without increasing MVO2. When the pressure overload is not eradicated in a variable amount of time the adaptative mechanisms slowly change to a pathologic process caused by collagen deposition in the interstitium of the heart. In advanced stages the remodeling process causes diastolic disfunction, myocardial ischemia, arrhythmias and death by heart failure or suddenly. This last stage is the real hypertensive heart disease.

[Left ventricular function in pure mitral stenosis. Hemodynamic echocardiographic study]. / La función ventricular izquierda en la estenosis mitral pura. Estudio ecocardiográfico hemodinámico.

We studied the left ventricular performance in 40 patients with pure mitral stenosis, using a M Mode Echocardiographic study. In 19% of the group the left ventricular function was abnormal, however, we were able to distinguish three subsets: small left ventricular dimension, normaland dilated. In the first two subsets, the cardiac performance was normal in almost all the patients (85%). In 15%, the left ventricular function was depressed, probably due to a restricting flow into the cavity, segmental atrophy and fibrosis caused by chronic mitral obstruction. In the last group (dilated left ventricle), the end-systolic dimension was abnormal in 71,4% of the patients. Our study suggests that the increased dimension of the left ventricle is accompanied by poor ventricular performance and represents an intrinsic trace of damage of the myocardium by the previous rheumatic carditis. The importance of detecting this last subset is emphasized due to the high incidence of impairment in left ventricular function. This detection could in some cases prevent the surgical treatment when this function is severely depressed.