Pseudomalfunction of a Beall mitral valve prosthesis in the presence of paravalvular aortic regurgitation.

Premature closure of a Beall mitral valve prosthesis is described in a patient with aortic prosthetic paravalvular regurgitation. Differentiation from valvular malfunction and diagnostic confirmation by means of cinefluoroscopy and simultaneous electrocardiography are discussed.

Mechanism responsible for the cardiovascular depressant. Effect of protamine sulfate.

The mechanism of protamine-induced hypotension and bradycardia was investigated in anesthetized, heparinized dogs. Several groups of animals with intact circulation were studied for their responses to protamine under control conditions and following the administration of various pharmacological agents. The parameters observed include femoral arterial pressure (FAP), central venous pressure (CVP), left ventricular pressure (LVP) and its rate of rise (dp/dt), left ventricular contractile element velocity of shortening (Vce), maximal Vce (V max) and cardiac output (CO). Various groups were studied under the following pharmacological conditions: autonomic cholinergic blockade by atropine; alpha and beta adrenergic receptor blockade using phenoxybenzamine and propranolol respectively; ganglionic and adrenal medullary block using hexamethonium, and depletion of endogenous histamine by means of compound 48/80. Another group was placed on total cardiopulmonary bypass thus isolating the heart from the peripheral circulation. The effect of protamine on the vascular tree alone was then observed by monitoring FAP before and after protamine administration. The findings indicate that the cardiovascular effects of protamine are produced by a direct effect on the myocardium and vascular tree.

Cardiovascular depressant effect of protamine sulphate: experimental study and clinical implications.

The mechanisms underlying protamine-induced hypotension and bradycardia were the subject of this investigation. Six groups of dogs with intact circulation were tested in controlled circumstances with various drugs. The following parameters were observed: femoral arterial pressure, central venous pressure, left ventricular pressure and its rate of rise, left ventricular contractile element velocity of shortening, maximal Vce, and cardiac output. The six groups were studied under these pharmacological conditions: ganglionic and adrenal medullary block with hexamethonium chlroide, postganglionic parasympathetic blockade by atropine sulphate, alpha and beta adrenergic receptor block by phenoxybenzamine and propranolol respectively, and depletion of endogenous histamine by compound 48/80 (a condensation product of p-methoxyphenethyl methylamine with formaldehyde). The last group was put on extracorporeal circulation to isolate the vascular tree from the heart. The effect of the drug on this isolated vasculature was observed by recording the femoral arterial pressure. Our findings show that the hypotension and bradycardia are produced by a direct effect of protamine on the myocardium and peripheral vascular system.