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Biomedical subjects

J P Snoeck

Publications and source records attributed to J P Snoeck.

8 recordsLinked to original sources
PubMed1994

Paradoxic pulmonary vasoconstriction in response to acetylcholine in patients with primary pulmonary hypertension.

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.

Acetylcholine↗
PubMed1992

Impaired endothelium-dependent cholinergic coronary vasodilation in patients with angina and normal coronary arteriograms.

The coronary vasomotor responses to selective infusion of graded concentrations (10(-6) to 10(-4) M) of acetylcholine into the left anterior descending artery were assessed by quantitative coronary arteriography in 24 patients with normal coronary arteriograms (12 patients with atypical symptoms and 12 patients with typical anginal pain) and 36 patients with coronary artery disease with different degrees of atherosclerosis of the left anterior descending artery. In the patients with normal coronary arteries and atypical chest pain, acetylcholine induced predominantly a vasodilator response, which was maximal during a 10(-5) M acetylcholine infusion. In contrast, in patients with coronary artery disease, acetylcholine caused dose-dependent vasoconstriction, which was observed even if the left anterior descending artery itself was smooth. Marked vasoconstriction was also induced in the patients with typical anginal pain and angiographically normal coronary arteries. In nine of these patients, this constrictor response was associated with anginal pain and electrocardiographic evidence of myocardial ischemia. Intracoronary administration of isosorbide dinitrate (1 mg) relieved the anginal pain and dilated all vessels. These data suggest that 1) patients with normal coronary arteriograms and angina pectoris manifest impairment of endothelium-dependent vasodilation similar to that observed in patients with overt coronary atherosclerosis; and 2) abnormal coronary vasoconstrictor responses resulting from this impairment may contribute to the pathogenesis of myocardial ischemia and angina in these patients.

Acetylcholine↗
PubMed1992

Paradoxical vasoconstriction as result of acetylcholine and serotonin in diseased human coronary arteries.

UNLABELLED: In experimental atherosclerosis, impairment of endothelium-dependent vasodilation results in an unmasking of potent vasoconstrictor responses to serotonin, a substance released by aggregating platelets. To determine whether similar changes occur in diseased human coronary arteries, the responses to selective intracoronary infusions of acetylcholine and serotonin (both endothelium-dependent vasodilators) and to isosorbide dinitrate (a dilator directly acting on the smooth muscle) were assessed by quantitative coronary arteriography in 16 patients with angiographically normal coronary arteries, in 10 patients with minimal (less than 30% narrowing) and in five patients with more advanced (greater than 50% narrowing) coronary atherosclerosis. Acetylcholine induced constriction in diseased coronary arteries, but in patients with normal coronary arteriograms, it caused dilatation in seven patients (smooth dilators) and constriction in nine patients (smooth constrictors). In the smooth dilators, however, serotonin evoked no significant changes (+1.4 +/- 4.1%), whereas in the smooth constrictors and in patients with diseased coronary arteries, serotonin caused dose-dependent constriction. The vasoconstrictor responses to serotonin were similar in patients with minimal (-26.5 +/- 4.7%) and more advanced atherosclerosis (-30.9 +/- 5.3%). In one patient with coronary artery disease, serotonin caused a temporary coronary occlusion. All other patients dilated in response to isosorbide dinitrate. The vasomotor responses to acetylcholine and to serotonin were thus shown to be completely in parallel. CONCLUSION: impairment of endothelium-dependent vasodilation unmasks potent vasoconstrictor responses to serotonin both in early and advanced coronary atherosclerosis. These changes may play an important role in the pathogenesis of a dynamic coronary artery stenosis.

Acetylcholine↗
PubMed1992

Angiographic coronary artery lesion morphology and pathogenetic mechanisms of myocardial ischemia in stable and unstable coronary artery disease syndromes.

The angiographic morphology of coronary artery stenoses was studied in 160 patients referred for diagnostic coronary arteriography. Three groups of patients were studied: 60 patients with stable angina, 78 patients with unstable angina and 22 patients with a recent myocardial infarction. Complex lesions were more frequently observed in patients with unstable angina (59%, p less than 0.001) and in patients with a recent myocardial infarction (54%, p less than 0.05) then in patients with stable angina (25%). Angiographic signs suggestive for the presence of intravascular thrombi were almost exclusively observed in the patients with unstable angina (34%, p less than 0.001) and in the patients with a recent myocardial infarction (27%, P less than 0.001) and were almost completely absent in the patients with stable angina (1.5%). The high prevalence of complex coronary artery lesion morphology and of intravascular thrombi observed in patients with unstable angina or with a recent myocardial infarction emphasizes the important role of intima disruption and of subsequent thrombosis in the pathogenesis of myocardial ischemia in those unstable syndromes of ischemic heart disease.

Angina Pectoris↗
PubMed1985

Temporary AVI pacing by chest wall stimulation.

Temporary atrial pacing (coded AVI pacing) has recently been proposed to assess atrial capture in patients with unipolar dual chamber pacemakers. This pacing mode can usually be achieved by programming the ventricular output to a subthreshold value. In patients with noncommitted bifocal pacemakers, AVI pacing can also be obtained by prolonging the programmed AV delay allowing for spontaneous conduction after atrial capture. However, in patients with prolonged AV conduction and a low aventricular stimulation threshold, ventricular stimulation cannot be prevented using the forementioned procedures. Using chest wall stimulation, we developed and tested a new method of temporary AVI pacing in patients with noncommitted DDD or DVI pacemakers.

Cardiac Pacing, Artificial↗