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Biomedical subjects

W H Qi

Publications and source records attributed to W H Qi.

8 recordsLinked to original sources
PubMed1992

[Electrophysiological effects of intravenous propafenone for treating atrial-ventricular nodal dual pathways reentrant tachycardia].

The acute electrophysiological effects of intravenous propafenone were studied through programmed electrical stimulation in 9 patients with atrio-ventricular nodal dual pathways reentrant tachycardia (AVNDP-RT). The results showed that propafenone prolonged significantly the effective refractory period of atrial ventricular nodal fast pathway (AVN-FP) in retrograde conduction and might further terminate the paroxysmal supraventricular tachycardia (PSVT). It is an effective drug for treating AVNDP-RT. Neither blood pressure dropping nor other side effects were observed.

Adult↗
PubMed1992

Hemodynamic assessment of intravenous Isosorbidi Dinitras in coronary heart disease.

This study investigates the systemic hemodynamic effects of intravenous Isosorbidi Dinitras, Isoket (ISDN) in 20 patients with coronary arterial disease to test the validity of the hypothesis concerning the relief of myocardial ischemia. Patients were eligible for the study if they had angina with coronary angiographic records or if they were cases of post-myocardial infarction. Before and after ISDN infusion the following measurements were recorded or calculated: heart rate (HR); systolic, diastolic and mean aortic pressure (ASP, ADP, AP); systolic and mean pressure of the left ventricle (LVSP, LVP); end-diastolic pressure in the LV (LVEDP); left ventricular contractility (dp/dt max); the double products (DP, HR x LVSP) and myocardial perfusion pressure in the LV (LVPP). After ISDN the ASP, AP and LVEDP decreased while HR, ADP, dp/dt and DP showed no significant changes. However, LVEDP was significantly decreased from 20 +/- 7 to 12 +/- 5 mmHg (P less than 0.01) with increased LVPP from 49 +/- 12 to 56 +/- 13 mmHg (P less than 0.01), which may be favourable for the relief of myocardial ischemia. There was no significant change of dp/dt max with decreased LVEDP after ISDN. It is suggested that the left ventricle can maintain normal performance at lower intracardial volume (preload) in these patients.

Adult↗
PubMed1991

Relationship between left ventricular end-diastolic compliance and abnormal Doppler mitral filling in patients with coronary artery disease.

Left ventricular end-diastolic compliance (LVEDC) and transmitral flow velocities were measured in 19 patients with coronary artery disease associated with hypertension and 10 normal subjects by LV catheterization and pulsed-Doppler echocardiography. LVEDC was much lower in the patient than in the normal subjects (P less than 0.01). The data showed that abnormal Doppler diastolic function such as elevated late diastolic peak flow velocity (PVA) and decreased LVEDC occurred in the patients at the same time. In addition, the negative correlation of PVA with LVEDC observed in normal controls but not in patients suggested that in patients with impaired diastolic filling, factors other than the decreased LVEDC itself must also participate in the development of diastolic dysfunction.

Aged↗
PubMed1989

[Estimation of intracellular free calcium concentration in patients undergoing digitalis treatment and in patients presenting digitalis toxicity].

Delayed afterdepolarizations occur under conditions in which there are large increase in the intracellular Ca and may be considered as one of the important mechanisms for digitalis-induced arrhythmias. Intraplatelet free calcium (Ca2i+) was measured in 25 patients, using the fluorescent indicator Quin-2. The patients included 15 with glycosides treatment (Group A) and 10 with arrhythmias indicating the presence of digitalis intoxication (Group B). The average Ca2i+ level in Group A was higher than the normal value but did not reach a statistical significance (170.8 +/- 9.09 vs 161.6 +/- 30.2, NS). The Ca2i+ level during digitalis toxicity in Group B was significantly higher than that in Group A (201.7 +/- 17.65 vs 170.18 +/- 91.09, P less than 0.01) as well as the normal value (P less than 0.01). With the disappearance of digitalis toxicity the Ca2i+ level was significantly decreased from 201.7 +/- 17.65 to 171.4 +/- 14.08 (P less than 0.001). Following the elimination of digitalis toxicity the increased digoxin concentration also declined. However, the decline of digoxin concentration did not correlate well with the decline of Ca2i+ (r = -0.57, P greater than 0.05). There is a close association between digitalis-induced arrhythmias and the change of Ca2i+ level, compatible with the tentative mechanism of delayed after depolarization (triggered activity). The poor correlation between the Ca2i+ level and digoxin concentration during the process of digitalis toxicity may suggest the presence of factors other than glycosides concentration to cause increased Cai2+ and arrhythmias.

Adult↗