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Biomedical subjects

O Patart

Publications and source records attributed to O Patart.

7 recordsLinked to original sources
PubMed1981

[Haemorrhagic necrosis of the digestive tract consecutive to massive digitalis intoxication (author's transl)].

A 60-year-old man under digitalis treatment for hypertensive heart tried to commit suicide by absorbing a 15 mg dose of digitoxin. Severe intestinal bleeding occurred 12 hours later, followed by pseudo-occlusive syndrome and ischaemia of the distal lower limbs. On abdominal incision the whole gut was found to be invaded by haemorrhagic necrosis and perforated on three points. The patients subsequently died of peritonitis. The responsibility of digitoxin in these events was demonstrated by the absence of any other cause of ischaemia, such as heart failure, shock, arrhythmia, consumption coagulopathy or use of sympathomimetic drugs. This case shows that the vasoconstrictor effect of digitalis, experimentally demonstrated but clinically controversial, is a reality, and that digitalis compounds are contra-indicated in patients with haemorrhagic necrosis of the digestive tract.

Digitalis Glycosides↗
PubMed1981

[The clinical diagnosis of aorto-coronary bypass occlusion (author's transl)].

The clinical profile of aorto-coronary bypass occlusion was drawn from a study of 49 patients with 56 occluded bypasses and 69 patients with 123 patent bypasses. All patients had undergone postoperative coronary arteriography or post-mortem examination. An anatomical cause of occlusion was retrospectively detected on the basis of pre-operative arteriographic findings or operation records in 82% of the cases, and on account of post-operative myocardial infraction (particularly significant when of late occurrence), residual angina and positive exercise tolerance test in 35%, 55% and 40% respectively of the cases. The last three criteria are of absolute diagnostic value when the arterial defects have been fully corrected by surgery.

Angina Pectoris↗
PubMed1979

[Hemodynamic changes during increasingly rapid atrial pacing].

The cardiac output (Qc), indices of left ventricular function in the isovolumic period (dp/dt/Pt), max, and during the ejection period (EF, VCF), the end diastolic and end systolic ventricular volumes, the speed of ventricular filing, the module of elasticity of the ventricular chamber (kp) and the end systolic pressure-volume relationships were measured in 20 patients (11 normal in group I and 9 with and apparently primary cardiomyopathy in group II) at rest and during progressively rapid atrial pacing. The Qc was lower and the indices of left ventricular function in the isovolumic and ejectional phases, the end systolic pressure-volume relationship and speeds of ventricular filling were decreased in group II: kp was the same in both groups of patients. At progressively higher heart rates the cardiac output slightly in both groups, the systolic volume decreased, (dp/dt/Pt) max increased, the ejection fraction and VCF were unaltered. The speeds of filling and kp were unchanged. The end systolic pressure-volume relationship increased. In group I the reduction in systolic volume seemed to be related to a greater reduction in the end diastolic volume than in the end systolic volume. In group II, the reduction of the systolic volume was related only to a reduction of the end diastolic volume.

Adult↗
PubMed1978

[Comparison of hemodynamic and coronary effects of 2 antianginal vasodilator drugs: nifedipine and trinitrine].

Twenty patients with coronary insufficiency had measurements taken while they were in normal rhythm (NR) and during atrial pacemaking (AP) before and after taking nifedipine (n: 12) or after intravenous perfusion of trinitrin (n: 8): measurements were taken of pulmonary capillary pressure (PCP), arterial femoral pressure (AFP), cardiac output (QC) and coronary sinus flow (QCS), coronary arterio-venous oxygen difference (DaVO2), myocardial oxygen consumption (MVO2) and the myocardial coefficient of extraction of lactates (K).--Under nifedipine in NR and AP, AFP was decreased and QC increased. QSC was increased in NR, but was not changed under AP. DaVO2 was shortened under both sets of conditions. MVO2 decreased only during AP. Nifedipine brought back to normal the lowering of K which occurred with pacemaking.--Under trinitrin, both in NR and under AP, AFP, PCP, QC, QSC and MVO2 were lowered. K and DaVO2 were unchanged.--A plethysmographic study in 13 patients showed that these haemodynamic effects could be explained by the arterial vasodilator action of nifedipine which occurred without changing the venous tone, and the mixed action of trinitrin.

Adult↗