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Biomedical subjects

M A Chiong

Publications and source records attributed to M A Chiong.

32 records · Page 2Linked to original sources
PubMed1979

Effects of glucose-insulin-potassium infusion on the angina response during treadmill exercise.

The effects of glucose-insulin-potassium (GIK) and placebo normal saline (S) infusion on treadmill-walking time to angina, ST depression, heart rate (HR), systolic blood pressure (SBP), rate pressure product (RPP), blood glucose (G), lactate (L) and free fatty acids (FFA) were studied in 14 non diabetic patients with exertional angina. For the whole group, the post-GIK walking time to angina (393 +/- 33 sec, mean +/- SEM) was greater than the values during control GIK (319 +/- 20 sec, p less than 0.02) and post-S infusion (334 +/- sec, p less than 0.05), but circulatory and ST responses were similar in post-GIK and post-S studies. 7 of the 14 patients experienced significantly greater improvement in exercise tolerance following GIK (467 +/- 39 sec) in comparison to control GIK (313 +/- 29 sec, p less than 0.001) and post-S infusion (334 +/- 32 sec, p less than 0.005) and exercised to a higher HR, SBP and RPP after GIK than after S infusion. At the onset of angina these patients had similar ST-segment depression before and after GIK but when ST segments were assessed after GIK at the same exercise duration when angina had occurred during the control and post-S studies, there was significantly less ST depression (p less than 0.01). Of the remaining 7 patients exercise tolerance following GIK deteriorated in 3, remained unchanged in 2 and increased by 12 and 48 sec in 2 patients in comparison to post-S values. Comparison of post-GUK and post-S values for G, L and FFA for the whole group showed significantly lower resting values of FFA and post-exercise values of G following GIK infusion. The differences in clinical and circulatory responses between patients who improved and those who did not improve following GIK were not related to the angiographically determined severity of coronary artery disease or to GIK-induced metabolic changes. Results suggest that some patients with angina pectoris do benefit from GIK infusion but the response in a given patient to this therapeutic modality is unpredictable.

Adult↗
PubMed1978

Metabolism of the isolated perfused rabbit heart. I. Responses to anoxia and reoxygenation. II. Energy stores.

Cardiac performance, substrate utilization, and creatine kinase (CK) release were studied in Langendorff rabbit hearts during aerobic perfusion, 25 min of anoxia, and 75 min of reoxygenation. In study I (n = 40), increasing glucose availability during aerobic perfusion enhanced substrate utilization without influencing cardiac performance, and this effect was not modified by insulin. Reoxygenation with glucose decreased CK (milliunits per millilitre) in the coronary sinus effluent but the best early recovery occurred in hearts protected with the 'cocktail' (see Table 1) during anoxia and perfused with glucose and insulin during recovery. This early recovery of performance was associated with transient higher CK loss, an effect that may have been related to one or more of the following factors: squeezing out of interstitial CK, heterogeneous anoxic injury to the myocardium, severe sarcolemmal damage, and preferential energy utilization by the contractile apparatus. In study II (N = 82), increasing recovery of cardiac performance was associated with increasing rate of CK loss (milliunits per minute) during reoxygenation. At 15 min of recovery, creatine phosphate (CP) and ATP stores were 400 and 50% of the aerobic group suggesting the presence of a defect in energy transfer from CP to the cytosolic ADP:ATP system. Thereafter, CP levels gradually declined while ATP reached a peak concentration of 85% of the aerobic group at 30 min. By the end of recovery, ATP stores were low at 23% of control, at a time when cardiac performance and the rate of CK loss were maximal. The significance of these depleted ATP stores remains to be elucidated.

Adenosine Diphosphate↗
PubMed1977

Effects of propranolol on the hemodynamic, coronary sinus blood flow and myocardial metabolic response to atrial pacing.

The hemodynamic, coronary sinus blood flow and myocardial metabolic effects of 0.15 mg/kg body weight of intravenously administered propranolol were studied in 19 patients with coronary artery disease and 6 normal patients. Atrial pacing was performed in all patients and produced angina in 15 of the 19 patients with coronary artery disease. In these patients propranolol reduced heart rate from 78 to 69 beats/min, cardiac index from 3.0 to 2.6 liters/min per m2 and left ventricular stroke work index from 47 to 43 g-m/m2; it increased total peripheral resistance from 24 to 28 units and lactate extraction from 16.3 to 22.5%. There was no significant change in mean arterial pressure, left ventricular end-diastolic pressure, coronary sinus blood flow or myocardial oxygen consumption. During a second pacing stress propranolol produced clinical improvement in 9 of the 15 patients who experienced angina initially. The improvement was associated with less severe abnormalities in S-T depression and left ventricular end-diastolic pressure, increased lactate extraction and no significant change in coronary sinus blood flow or myocardial oxygen consumption. Thus, propranolol appears to be capable of modifying the anginal threshold as determined with atrial pacing, and the clinical response appears to be independent of global changes in coronary sinus blood flow and myocardial oxygen consumption.

Angina Pectoris↗
PubMed1976

The protective effect of glucose-insulin-potassium on the response to atrial pacing.

The effects of glucose-insulin-potassium infusion (GIK) on atrial pacing-induced angina, ST depression, abnormal left ventricular end-diastolic pressure during pacing interruption (LVEDPi) and lactate metabolism (L), were studied in 18 patients: ten had angina during pacing = Ischemic group, and eight (5 normals and 3 with coronary artery disease) remained asymptomatic = Nonischemic group. The study consisted of 8-10 minute periods of control, pacing and recovery, before and after GIK. No untoward effects were observed. Comparison of the pacing responses (GIK vs pre-GIK states) showed that during GIK, angina occurred in only 4 patients, while significantly less severe changes were observed in ST depression (1.4 +/-0.5 vs 2.4 +/- 0.4 mm) and LVEDPi (16 +/- 3 vs 23 +/- 3 mm Hg). Lactate extraction was also higher (8.1 +/- 10.9 vs -5.2 +/- 11.1%), but not significantly so, although L became normal in 4 subjects and improved in another. These results indicate that GIK infusion was well tolerated and had a beneficial effect on pacing-induced myocardial ischemia.

Adult↗
PubMed1975

Metabolic indicators of myocardial ischemia in man.

Myocardial metabolism had been studied in 54 patients with continuous sampling of arterial (A) and coronary sinus (CS) blood during 8- to 10-min periods of control in sinus rhythm, rapid atrial pacing and recovery. The results showed that 17 subjects were normal or had insignificant coronary artery disease (CAD; nonischemic group = NI); 37 patients had significant CAD (ischemic group = 1) and developed clinical, hemodynamic, and electrocardographic evidence of myocardial ischemia during pacing, characterized by angina, elevated left ventricular end-diastolic pressure, and depressed ST segments. During pacing-induced ischemia the following metabolic abnormalities were detected: (1) myocardial anaerobiosis indicated by lactate % uptake ((A-CS)/AS X 100) of -17.2 +/- 5.0% (mean +/- SE); (2) myocardial loss of K+ suggested by an A-CS difference of -0.25 +/- 0.08 mEq/liter (N=18); (3) small but significant loss of inorganic phosphorus (Pi) of -1.0 +/- 1.4% (N=18); and (4) elevation of CS blood creatine phosphokinase activity (N=5). These metabolic abnormalities were temporally related to the other manifestations of myocardial ischemia and were not seen in the NI; Lactate production and Pi loss occurred in 75 and 55% of the IG, respectively, suggesting that accelerated anaerobic glycolysis was the best indicator of myocardial ischemia in man. K+ loss was an unreliable index in this experimental situation, since tachycardia alone caused significant K+ egress from the heart. Lactate production and K+ loss were reduced by nitroglycerin, which abolished angina and improved hemodynamics and electrocardiographic manifestations. That these metabolic abnormalities were not observed in all 1 patients may have been related to methodology, the random distribution of CAD, and the fact that the chemical composition of the CS blood reflects the metabolic balance of both well oxygenated and ischemic areas of the myocardium.

Adult↗