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Metabolic response to prolonged reduction of myocardial blood flow distal to a severe coronary artery stenosis.

Limited data are available concerning the effects of mild-to-moderate, sustained reductions of coronary blood flow on myocardial aerobic metabolism. This study tested the hypothesis that a sustained flow reduction distal to a severe coronary artery stenosis may be well tolerated (after the initial insult is passed) because of gradual improvement in the balance between myocardial oxygen supply and demand. Studies were performed in eight sedated, closed-chest domestic swine that were instrumented with an artificial coronary arterial stenosis (80% diameter reduction). Hemodynamics, regional myocardial blood flow and oxygen, lactate, acid, and base metabolism were measured before stenosis and at 5, 20, 60, 120, and 180 minutes after stenosis insertion. Regional myocardial function (ultrasonic length sensors) was measured serially during 2 hours in three additional swine. After stenosis placement, endocardial and transmural flows declined (p less than 0.05) compared with flows before stenosis (from 1.54 +/- 0.37 to 0.73 +/- 0.24 ml/min/g [mean +/- SD] and from 1.44 +/- 0.31 to 1.19 +/- 0.25 ml/min/g, respectively). Thereafter, flows remained unchanged for the duration of the study. Similarly, prestenosis heart rate (135 +/- 7 beats/min), aortic mean pressure (113 +/- 17 mm Hg), and tension time index (27.1 +/- 3.6 mm Hg.sec) remained constant for the duration of the study. In contrast, regional coronary venous pH declined (p less than 0.05) compared with prestenosis levels (7.35 +/- 0.02) 5 minutes after stenosis (7.28 +/- 0.04), but it returned to prestenosis levels during the next hour. Regional coronary venous PCO2 exhibited a similar pattern (i.e., acute increase during poststenosis with gradual return to prestenosis levels).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis in patients with unstable angina.

To determine whether a reduction in myocardial oxygen demand or an increase in coronary blood flow or both are responsible for the salutory effect of intraaortic balloon counterpulsation (IABP) in relieving medically refractory angina, we assessed these variables in six patients in whom IABP was required for relief of myocardial ischemia. IABP decreased the rate7pressure product and aortic enddiastoliczpressure, and the peak systolic aortic pressure and regional myocardial oxygen consumption declined in- all but one patient. Peak and mean aortic diastolic pressures increased. Changes in regional coronary blood flow paralleled changes in peak systolic aortic pressure (r = 0.92, p < 0.007). Thus, relief of angina during IABP could not be ascribed to an increase in regional coronary blood flow. Reduction of myocardial oxygen consumption is the most likely mechanism by which IABP relieves myocardial ischemia in patients with unstable angina pectoris.

Effect of a reduction in blood viscosity on maximal myocardial oxygen delivery distal to a moderate coronary stenosis.

This study tested the hypothesis that a reduction in blood viscosity by means of isovolumetric hemodilution will permit an increase in maximal oxygen delivery to myocardium distal to a moderate coronary arterial stenosis. It is known that blood viscosity is a determinant of resistance to blood flow at both the stenotic and the arteriolar levels. Accordingly, a reduction in blood viscosity could exert a favorable influence on maximal myocardial oxygen delivery in the setting of stenosis, provided that the oxygen-carrying capacity of the blood is not compromised excessively. Closed-chest, sedated domestic swine (n = 8) were instrumented with an artificial coronary arterial stenosis that reduced vessel diameter by 64%. Measurements of hemodynamics, regional myocardial blood flow (microspheres), lactate and oxygen metabolism, and whole blood viscosity were made at control and after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Next, albumin/saline solution was given intravenously to reduce the animals hematocrit by approximately 50%. Repeat measurements of all experimental variables were then made at a second control and again after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Myocardial blood flow (ml/min/g) distal to the stenosis increased from 1.52 +/- 0.21 (mean +/- 1 SD) to 4.10 +/- 0.86 in response to adenosine (peak dose) before hemodilution (p less than .01) and from 2.07 +/- 0.59 to 4.08 +/- 0.93 (p less than .01) after hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation to the stress of tachycardia in patients with coronary artery disease: insight into the mechanism of the warm-up phenomenon.

Adaptation to exercise or the warm up phenomenon has been observed in some patients with angina pectoris. To investigate adaptation, eleven patients with exertional angina pectoris and angiographic evidence of coronary artery disease underwent two identical bouts of sequential tachycardia stress separated by a brief recovery period. Manifestations of ischemia were less during the second stress, as evidenced by a reduction in the severity of angina pectoris, less ST segment depression, and improved lactate extraction. Peak coronary blood flow during the second stress (81 +/- 20 ml/min) was not significantly different from that during the first (95 +/- 32 ml/min). Regional myocardial oxygen consumption, however, was significantly (p = .03) lower during the second stress (8.8 +/- 2.4 ml O2/min) when compared with the first (11.4 +/- 3.0 ml O2/min). Thus, patients with coronary artery disease can develop anginal tolerance to the stress of tachycardia similar to that observed after repeated bouts of exercise. A relative reduction in myocardial oxygen consumption, rather than an increase in coronary blood flow, appears to account for this phenomenon.

Prediction of long-term clinical outcome with final translesional pressure gradient during coronary angioplasty.

The final translesional pressure gradient measured during coronary angioplasty correlates with immediate angiographic and clinical results. Whether the pressure gradient is of value in predicting late clinical outcome has not been determined. We therefore obtained complete follow-up information on 159 patients with single-vessel disease who underwent successful coronary angioplasty. Mean follow-up time was 15 +/- 10 months. The occurrence of repeat angioplasty, coronary bypass surgery, recurrent anginal chest pain, or a positive postangioplasty stress test were considered clinical events indicative of late failure. Of the variables age, gender, initial and final translesional pressure gradient, extent of initial and final arterial narrowing, site of dilatation, type of balloon catheter used, number of inflations, and maximal inflation pressure, only the final translesional pressure gradient was predictive of late failure when analyzed by multivariate techniques. Thus, the final translesional pressure gradient is of value in predicting both immediate and late outcome after coronary angioplasty.

Economic effects of community versus hospital-based faculty pneumonia care

To compare the length of stay and charges for patients with pneumonia admitted in 1995 to the teaching and nonteaching services of a Northeastern teaching hospital, we reviewed the charts of 237 patients. Patients cared for by hospital-based generalists working with housestaff (teaching service) were discharged more quickly and with lower or equivalent charges than patients cared for by community-based attending physicians working either with housestaff (private teaching service) or alone (nonteaching service). Academic teaching services staffed by general medicine faculty may provide efficient inpatient pneumonia care.

Assessment of coronary flow reserve using digital angiography before and after successful percutaneous transluminal coronary angioplasty

Important alterations of coronary blood flow and coronary flow reserve occur during percutaneous transluminal coronary angioplasty (PTCA). This study evaluated these alterations using digital subtraction angiography. Coronary flow reserve was determined before and after successful PTCA in 20 patients with 1-vessel coronary artery disease (CAD). Ten other patients with angiographically normal coronary arteries, normal exercise electrocardiographic responses and normal cardiac structure also were evaluated. Coronary flow reserve was calculated as the ratio of papavarine-induced hyperemic flow to basal flow. Flow reserve for the stenotic artery in patients who underwent PTCA was 1.6 +/- 0.2 (mean +/- standard error of the mean) (range 0.9 to 3.9, n = 20). After successful PTCA, flow reserve for this artery increased to 3.1 +/- 0.2 (range 1.7 to 5.2, n = 20) (p less than 0.0001 vs before PTCA). Flow reserve for adjacent nonstenotic, nondilated arteries was 2.6 +/- 0.2 (range 1.4 to 4.5, n = 13). Coronary flow reserve in the stenotic arteries before PTCA was far below normal. In addition, both successfully dilated arteries and nondilated, nonstenotic arteries in these patients with CAD had flow reserve values smaller than those in the patients with normal arteries (4.8 +/- 0.6, range 2.3 to 12.6, n =22) (p less than 0.01). These findings suggest that digital angiographic determinations of coronary flow reserve can reveal important alterations of individual artery vasodilatory capacity. The data suggest that although an epicardial coronary in a patient with CAD may appear angiographically normal, flow reserve remains impaired due to abnormalities as yet undefined.

Angiographic findings when chest pain recurs after successful percutaneous transluminal coronary angioplasty

Angiographic and clinical characteristics of 102 consecutive patients who underwent coronary cineangiography for assessment of recurrent angina pectoris after successful percutaneous transluminal coronary angioplasty (PTCA) were reviewed. Based on angiographic findings, patients were classified as having restenosis (n = 63), development of new, significant coronary stenosis (n = 15), incomplete revascularization (n = 9) or no significant coronary artery disease (n = 15). Eighteen clinical and technical characteristics of the study group were analyzed as predictors of angiographic outcome. The groups did not differ in terms of age, gender, number of inflations performed, peak inflation pressure or in the pre- or post-PTCA stenosis or gradient. The time from PTCA to onset of recurrent angina was the most powerful predictor of angiographic outcome. Patients in whom symptoms developed within 1 month of PTCA usually had incomplete revascularization or no coronary narrowing. Restenosis was the most common explanation for chest pain 1 to 6 months after PTCA. Angina recurring more than 6 months after PTCA was usually due to development of new, significant coronary artery narrowings.

Restoration of normal coronary hemodynamics and myocardial metabolism after percutaneous transluminal coronary angioplasty.

Regional coronary blood flow and myocardial metabolism were evaluated in a patient who underwent percutaneous transluminal coronary angioplasty (PTCA). Angioplasty increased coronary luminal diameter and reduced trans-stenotic gradient. Before PTCA, angina pectoris developed during sustained rapid atrial pacing and was associated with abnormal lactate metabolism and a mild increase in coronary flow and myocardial oxygen consumption. After PTCA, angina was absent during pacing and lactate extraction was preserved. Coronary flow and oxygen consumption were increased to a greater degree than before PTCA. The temporal response of changes in coronary blood flow due to an abrupt increase in heart rate was also evaluated. Floow reached peak value more rapidly after PTCA. These observations suggest that PTCA may result in improved regional coronary blood flow and restoration of normal flow regulatory mechanism and myocardial metabolism.

Ischemia-induced impairment of left ventricular relaxation: relation to reduced diastolic filling rates of the left ventricle.

An investigation was performed in order to better define the cause of reduced diastolic filling rates of the left ventricle (LV) observed in the setting of acute myocardial ischemia. Seven closed chest, anesthetized pigs were instrumented by placing a micromanometer-tip catheter in the LV and a balloon tip catheter in the midportion of the left anterior descending coronary (LAD) artery. The animals red blood cells were labeled with technetium-99m and LV time-activity curves obtained by means of a computer-controlled, nonimaging cardiac probe (collimated, 3.5 cm DIA, sodium iodide crystal). Nuclear data obtained simultaneously with LV pressure data were used to evaluate diastolic pressure-count rate (i.e., volume) relations of the LV under control conditions and at 5 and 10 minutes after balloon occlusion of the animals LAD. Diastolic filling rates, the time constant (“T”) of ventricular relaxation, the chamber passive stiffness constant (“K”), and maximum negative left ventricular DPDT were computed for each experimental condition. Maximum negative DPDT decreased compared with control (1690 + 699 mm Hg/sec; mean ± 1 SD) at both 5 minutes (1040 ± 493, p < 0.01) and 10 minutes (1360 ± 588, p < 0.05) after occlusion. Likewise “T” was prolonged versus control (45.3 ± 6.4) at both 5 minutes (56.8 ± 12.8, p < 0.01) and 10 minutes (54.0 ± 8.7, p < 0.05) after occlusion. In contrast both “K” and calculated left ventricular pressure at zero counts (i.e., volume) remained constant throughout the study. Left ventricular end-diastolic pressure also did not change significantly during the study. The mean, maximal, and mid to late LV diastolic filling rates all were prolonged significantly (p < 0.05) versus control at 5 minutes and 10 minutes after occlusion. The rate of early diastolic filling of the LV did not change significantly during the study, although it tended to decline along with the other rates. Thus, ischemia-induced changes in diastolic filling rates may be seen in the absence of changes in left ventricular chamber stiffness, and ischemia-induced impairment of left ventricular relaxation alone is sufficient to reduce the rate of diastolic filling of the LV.