By Robert Charlier
If the varied healing acquisitions of the previous few years have enriched very diversified fields of human pathology, it does look that coronary pathology has been given very distinct consciousness, as witness the wide range of antianginal medicinal drugs put on the disposal of the clinical occupation. there are lots of causes for this scenario, one in every of them most likely being that the medica tions successively proposed don't absolutely fulfill the practitioner and one other that the whole variety of participants being affected by the clinicaI manifestations of heart illness bargains, by way of its measurement, an unlimited revenue power for the pharma ceuticaI undefined. This box of purposes opens up such customers that it has inspired a prolific quantity of festival among a number of examine laborato ries, and it really is no exaggeration to claim that each significant enterprise has its individuaI anti anginaI drug in its healing cataIogue. another issue has aIso contributed vastly to this proliferation of medi cinal arrangements meant for the remedy of angina pectoris: this is often the quick boost in our knowIedge of the physiopathoIogy of angina, which in flip has produced originaI innovations of pharmacological and biochemical learn. accordingly, there have emerged new ingredients whose motion mechanisms have claimed to be most suitable to the cardiovascular issues accountable for cardiac discomfort.
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Extra resources for Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics
In eontrast, however, the patients with angina during pacing showed no fall in left ventrieular enddiastolle pressure in the faee of similar reduetions in stroke work. This abnormaI pressure eould be in part due to deereased eompllance of the isehaemie ventriele, but it is more reasonable to eonsider that it is operating on a depressed funetional eurve. With interruption of pacing, the heart rate returned abruptly to normal and, assuming no ehange in eardiae index, there was an inerease in left ventrieular stroke work .
The proof that a clinically improved angina subject, whatever the method used to achieve this, does not experience angina pain even at higher effort heart rate because the critical level of oxygen consumption by his myocardium is not reached has been provided by FRIeK et al.  who show that, during the speedup in heart rate produced by atrlal pacing bringing the normal rate up to almost double, the angina subject on nitroglycerin, whilst not suffering any heart attack, does not reach the myocardial oxygen consumption level (measured by the SARNOFF tension-time index) at which, in the absence of nitroglycerin, the angina pain occurs.
R : values at rest. E: values during exercise. (MESSER and NEILL, 1288) Patients presenting coronary insufficieney reveal the following eharaeteristics during effort: myocardial oxygen eonsumption increases to a greater extent than in the case ofnormal subjeets 6 • Coronary flow increases largelyin the same manner as for healthy subjeets, a faet important in itself whieh has sinee been eonfirmed  and whieh, aeeording to eertain authors , is in faet eharacterised by a greater inerease than is the ease for normal subjeets 8 • But, and this more than anything else distinguishes the anginal from the healthy subjeet, the oxygen content of the coronary venous blood is over 20% less [1288, 1842, 1953].
Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics by Robert Charlier