Robert Charlier's Antianginal Drugs: Pathophysiological, Haemodynamic, PDF

By Robert Charlier

ISBN-10: 3642651658

ISBN-13: 9783642651656

ISBN-10: 3642651674

ISBN-13: 9783642651670

If the various healing acquisitions of the prior few years have enriched very diversified fields of human pathology, it does look that coronary pathology has been given very precise awareness, as witness the wide range of antianginal medicinal drugs positioned on the disposal of the scientific occupation. there are many factors for this scenario, one among them most likely being that the medica tions successively proposed don't absolutely fulfill the practitioner and one other that the entire variety of participants struggling with the clinicaI manifestations of heart affliction deals, via its dimension, an enormous revenue power for the pharma ceuticaI undefined. This box of functions opens up such clients that it has inspired a prolific quantity of pageant among a variety of learn laborato ries, and it really is no exaggeration to claim that each significant enterprise has its individuaI anti anginaI drug in its healing cataIogue. a different issue has aIso contributed significantly to this proliferation of medi cinal arrangements meant for the therapy of angina pectoris: this is often the swift boost in our knowIedge of the physiopathoIogy of angina, which in flip has produced originaI innovations of pharmacological and biochemical study. accordingly, there have emerged new elements whose motion mechanisms have claimed to be most fitted to the cardiovascular problems accountable for cardiac discomfort.

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Extra info for Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics

Example text

Marked rise in blood pressure (systolle and diastolle) and heart rate [352, 1245]. Hypertension and taehyeardia unduly inerease the oxygen needs of the isehaemie eardiae musele, with the result that the latent ehronie myoeardial hypoxia turns to aeute hypoxia, the eause of the angina attack. These modern pathogenie eoneepts of the angina syndrome, whieh are based on widely doeumented pathophysiologieal observations remarkable for their eon14 This observation has enoouraged certain surgeons [501] to implant a paoemaker on the oarotid sinus nerves, whioh the patient oan bring into play whenever the need is felt (for details, see p.

During exertional angina, the average left ventrieular end-diastolle pressure rose from 8 to 32 mm Hg and the stroke work fell. This signifies that the isehaemie left ventricle was operating on a depressed ventrieular funetion eurve. The elevated left ventrieular end-diastoHe pressure may have been due in part to deereased eompllanee during myoeardial isehaemia but was probably related more to an augmentation in left ventrieular volume. Such a ehange would inerease myoeardial fiber length whieh, by the LAPLACE relation, would raise oxygen eonsumption.

5 pg/ min for 15-20 min causes in the coronary patient with significant stenotic or occlusive lesions disclosed by coronary arteriography (whose indications are in excellent eorrelation with post-mortem anatomicallesions, 1854), an increase in cardiac output and myocardial oxygen consumption, together with a 37 % rise in coronary flow, secondary to the increase in the metabolic needs of the myocardium [1854]. Since the increase in coronary flow is not accompanied by changes in blood pressure, adrenaline may thus be considered as a vaso-dilator according to the commonly accepted criteria [732].

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Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics by Robert Charlier

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