[Myocardial ischemia in aortic stenosis]. / La isquemia miocárdica en la estenosis aórtica.

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.

[Hemodynamic study in hypertensive cardiopathy under ischemia induced by atrial stimulation in the absence of fixed coronary obstructions]. / Estudio hemodinámico en la cardiopatía hipertensiva bajo isquemia inducida por estimulación auricular en ausencia de obstrucciones coronarias fijas.

With the purpose to study the haemodynamic changes that occur with myocardial ischaemia induced by atrial pacing (AP) in hypertensive heart disease, we studied 7 patients with such condition, all of them with a long time history of systemic hypertension, electrocardiographic signs at rest of left ventricular hypertrophy and ST-segment depression, at least of 0.5 mm. All the patients showed normal coronary arteries in angiocardiogram. AP was started 10 beats above the basal heart rate with increments of 10 beats every 2 minutes until a ST-segment depression at least of 2 mm was obtained which occurred in all the cases studied. After every 2 minutes of AP a simultaneous 12-leads electrocardiogram recording and left ventricular and aortic pull-back pressure were obtained. At the desired end point the AP was abruptly stopped and the same parameters were registered at 3, 5, 10 and 15 minutes until recovery. During AP the left ventricular systolic pressure (LVSP) did not show any significant change, with the exception of a patient who experienced angor pectoris during the proceeding. The left ventricular end-diastolic pressure (LVEDP) increased in 3.4 +/- 1.7 mmHg, change that was statistically significant (p less than or equal to 0.01) but not hemodynamically important since only in one patient it increased above the normal levels (from 13 mmHg basal to 17 mmHg during AP). In contrast, LVEDP markedly rose above normal when AP was stopped. It is concluded that neither LVEDP nor LVSP play an important role in the genesis of the ST segment depression seen in these patients. It is showed that, similar as in patients with obstructive coronariopathy, these cases work on a depressed Starling curve during AP and its recovery for what is thought that the functional meaning of ischaemia for both entities is similar no matter that their pathogenetic mechanisms are different.