Miguel A. Chiong

The Effect of Ischemia and Alterations of Heart Rate on Myocardial Potassium Balance in Man

Myocardial electrolyte balance and lactate metabolism were studied in 30 patients before, during, and after a period of atrial pacing utilizing a continuous automated sampling technic with simultaneous electrocardiographic and hemodynamic observations. Eight patients with coronary artery disease who had no symptoms during pacing and four normal subjects demonstrated myocardial potassium loss but no abnormalities in lactate metabolism, the electrocardiogram, and hemodynamics during pacing. Myocardial potassium loss was correlated with increments in heart rate and was followed by potassium uptake during the post-pacing period. Eighteen subjects developed angina during pacing associated with hemodynamic and electrocardiographic abnormalities. This ischemic group showed significantly greater myocardial potassium loss during pacing than the non-ischemic group, and this was closely associated with myocardial lactate production at a ratio of 1 mEq of potassium being lost for each 2 millimoles of lactate produced. Increased acidity of coronary sinus blood also accompanied potassium loss during ischemia. No significant changes were seen in sodium balance in either group during the study.

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.

The spectrum of unstable angina: Prognostic role of serum creatine kinase determination

A prospective study of 199 patients with unstable angina pectoris was undertaken to assess whether frequent serial sampling of serum creatine kinase (CK) was useful in predicting prognosis. Nineteen percent of the patients had transient CK elevations suggestive of a small myocardial infarct that was outside the detective ability of conventional electrocardiographic and enzymatic determinations. These patients had a 1 year mortality rate of 16 percent, which was significantly higher than that in the remaining patients (Fishers exact test p = 0.05). Furthermore, the recurrence rate of myocardial infarction (14 percent) in the patients who had transient CK elevation was significantly greater than that (2 percent) in those who did not have CK elevation (Fishers exact test p = 0/01). These data suggest that frequent serum CK sampling in the first 48 hours after admission for unstable angina has prognostic value and that persons with CK elevation may warrant a more aggressive approach to investigation and management.

Effects of low and high glucose in a glucose-insulin-potassium infusion on hemodynamics and exercise tolerance in patients with angina pectoris.

SUMMARYThe effects of infusion of normal saline (NS) and glucose-insulin-potassium (GIK) with either low or high G concentrations on hemodynamics and exercise tolerance were studied in patients with angina pectoris. Studies were performed at rest and during exercise, twice before and once after one of the infusions. Eleven patients (low-G GIK group) received 150 ml of GIK solution that contained 15 g G, 8 U I, and 12 mEq KCI; 10 patients received 150 ml NS; and seven patients (high-G GIK group) received 1.5 g/kg of G orally followed by a 100 ml infusion that contained 0.5 g/kg G, 1.5 U/kg I, and 10 mEq KCI.Before infusion, left ventricular end-diastolic pressure (LVEDP) was higher during the first exercise period (Ex1) than during the second exercise period (Ex2), but the exercise time to angina did not change significantly. After NS, exercise time to angina, hemodynamics and G levels were similar to the preinfusion Ex2 values.After low-G GIK infusion, G levels increased from 99 to 140 mg/dl (p < 0.01), but the exercise time to angina did not change significantly from the preinfusion Ex2 values. Only two of the 11 patients exercised for a longer period of time and had less ST-segment depression. However, LVEDP during exercise after low-G GIK infusion was lower compared with the preinfusion Ex2 values (18 vs 23 mm Hg, p < 0.02).After high-G GIK infusion, G levels increased from 109 to 331 mg/dl (p < 0.01), but exercise tolerance decreased from a mean preinfusion (EX2) value of 159 to 74 seconds (p < 0.01) after this infusion.These studies show that while low-G GIK had variable effects on exercise tolerance and reduced LVEDP during exercise-induced angina, high-G GIK had detrimental effects. Therefore, increasing substrate (G) availability had no beneficial effects on supine exercise tolerance in patients with angina pectoris.

Clinical, hemodynamic and metabolic responses during pacing in the supine and sitting postures in patients with angina pectoris

Abstract Hemodynamics during sinus rhythm and pacing-induced angina were studied in the supine and sitting positions in 12 patients with coronary artery disease. During sinus rhythm, left ventricular end-diastolic pressure, cardiac index, stroke index and left ventricular stroke work index were lower and heart rate was higher in the sitting position. During pacing, left ventricular end-diastolic pressure, stroke index and left ventricular stroke work index decreased, whereas pulmonary arterial mean pressure, mean pulmonary capillary wedge pressure and brachial arterial systolic and mean pressure remained unchanged in both positions. During pacing, angina was experienced by 12 patients in the supine and 10 patients in the sitting position. Chest pain was less severe and the pacing rates required to induce angina were higher in the sitting position (159 ± 3versus 132 ± 4 beats/min, P

Quantification of myocardial infarction: template model for serial creatine kinase analysis.

A self-modeling procedure was used to develop a template g(z) from the serial creatine kinase (CK) release in 32 patients with acute myocardial infarction. An additional 16 patients were used as an extrinsic test of the template model. For a given patient the fitted CK curve y(t) is related to the template g(z) by the expression -y(t)= /31g(t 2) + 03, where /, is equal to the peak height of the CK transient above background, 4, /2 is the time at which CK begins to rise, /3 iS the time taken for CK to rise to its maximum value. Calculations of infarct size using the template and a numerical estimate yielded values of 34.6 g-Eq and 33.5 g- Eq, respectively, with good agreement (r = 1.00). Comparisons of all point numerical estimations of infarct size with early point predictions revealed that the template and lognormal models performed equally well with 7 and 6 points; however, the template model was superior with 5 and 4 points. The template model also provides insight into the CK time activity curve. In particular, total CK activity and hence infarct size, are shown to be proportional to the peak of the excess CK curve, and the time course of CK appearance is revealed by the appearance and cumulative appearance functions.We found a high correlation between all point estimates of completed infarct size and a linear estimate obtained by fitting a straight line to the ascending portion of the CK curve.

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.