Stable Angina Pectoris: Regional Myocardial Ischemia and Insufficiency, Intersegmentary Confrontation and Cardiotonic Therapeutic

 Quintiliano H. de Mesquita, M.D.

The coronary atherosclerosis in the long run produces myocardial disease through the frequent angina pectoris crisis, developed by exertion or emotion, provoking transitory regional myocardial insufficiency (Tennant, R. and Wiggers, C.J. – Am. J. Physiol., 1935; 112: 351 and Mesquita, Q.H. de, 1972 – Annals of 28° Congress of Brazilian Cardiology Society).

The regional myocardial insufficiency leads to the development of changes in the myocardial structure called by Harrison, T.R. (Am. Heart J., 1965; 69: 100) as asynergic myocardial regions, coronary-dependent, characterizing the myocardial deficiency indicated by Koetter et al (Am. J. Cardiol., 1978; 42: 563) in the stable angina pectoris.

According the Myogenic Theory defended by us a myocardial pathology with well characterized aspects due to the involvement of 1, 2 or 3 myocardial coronary-dependent segments, induces to a functional disagreement between the ischemic and non ischemic areas, during the angina pectoris crisis.

Consequently, when occurs a provoked ischemia in the case of 1 coronary artery involved, the dependent region becomes inactive while the other 2 are hiperactivated, overloading the affected area; demonstrating in this way a clear pathological disharmony, resulted from an intersegmentary confrontation. Differently occurs in case of processes with 2 or 3 coronary arteries involved, with a marked participation of myocardial coronary-dependent segments; during the angina pectoris crisis, in this case, is recorded a clear pathological harmony practically without harmful intersegmentary confrontation.

 Based in the Myogenic Theory we established since 1972 the use of cardiotonics (digitalis or proscilaridine A) for stable angina pectoris. The permanently and lifetime protection and guarantee for the deficient myocardium, provided by cardiotonics also allows to an overleveling in contractility, annulling in this way the intersegmentary confrontation.

In a comparative study realized during 17 years in our private clinic with patients using cardiotonics for stable angina pectoris after the M.I. versus a similar group of patients which didn’t used cardiotonics we obtained a mortality result of 2.6 times less, in favor of the first group. The mortality in the first group had an average with patients around 70 years old and the mortality of second group had an average with patients around 64 years old.

Our unit has also followed, during the period 1972–1979, 562 patients treated after the M.I. with digitalis or proscilaridine at the outpatient department of Matarazzo Hospital in São Paulo, occurring a mortality of 16.1 % (2.3 % per year) with an average around 59 years old. The patients treated with cardiotonics in our private clinic and at the Matarazzo Hospital belonged to different levels in culture and social economic classes.

It was observed that in patients submitted to cardiotonic therapeutic, the abrupt stopping of its use may cause an evolution after certain time to unstable angina pectoris, myocardial infarction or sudden death. That behavior seems to what was verified in case of stable angina pectoris treated by beta blockers where happens similar complications after 2 – 21 days.

While using cardiotonics the leveling of myocardial segments are based in contractility, in case of beta blockers use the leveling of myocardial segments are based in hypocontractility with the annulment of the intersegmentary confrontation in both cases.

 The result of this annulment is of absolute protection with the cardiotonics use and just to play for time in case of beta blockers use, without avoiding in the second situation the occurrence of unstable angina pectoris and acute myocardial infarction, which finally tends to occur.

 With the interruption of the annulment effects of the intersegmentary confrontation, using any one of these drugs, it is easy to understand the origin of complications caused by to expose the unprepared coronary-dependent segments to an physical and direct overloading as according the pathophysiological mechanisms preconized by the myogenic theory.

We have recorded cases of unstable angina pectoris developed by the simultaneous use of cardiotonics and beta blockers, easily controlled by the suspension of the last one.

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