SUMMARY The effect of coronary artery bypass grafts on left ventricular performance was evaluated by analyzing preoperative (preop) and postoperative (postop) biplane left ventriculograms of 37 patients who were restudied at a mean of 13 months after operation. Eighty-two percent of the grafts were patent. Segmental wall shortening and segmental shortening velocities (mea Vcf) in the anterior, inferior and lateral regions of the left ventricle were compared in four groups: 1) regions with patent grafts and normal preop shortening, 2) regions with patent grafts and preop asynergy, 3) regions with occluded grafts and 4) ungrafted regions. In the 38 regions with preop normal shortening and patent grafts, shortening and shortening velocities were unchanged postop. In the 13 regions with preop asynergy and patent grafts, % shortening increased 22 + 8 (P < 0.01) and mean Vd, increased 0.82 ± 34 lengths/sec, (P < 0.025). In the 13 regions with occluded grafts, % shortening decreased 6 ± 3 (P < 0.05) and mean Vcf decreased 0.24 ± 0.11 lengths/sec (P < 0.025). In the 28 regions which were ungrafted, there was no change in shortening, while mean V,r decreased 0.56 ± 0.22 lengths/sec (P < 0.025). The effect of bypass grafts on global ventricular performance as measured by the ejection fraction (EF) was examined in patients with all patent grafts and normal preop wall motion, patients with all patent grafts and preop asynergy, patients with one or more occluded grafts and all patients combined. In the 11 patients with all patent grafts and normal preop wall motion, the EF was unchanged (0.74 0.03 preop and 0.71 0.02 postop; P = NS), while the EF increased in the 11 patients with all patent grafts and preop asynergy (0.53 ± 0.02 preop and 0.65 ± 0.05 postop; P < 0.05). In the 11 patients with one or more occluded grafts, the EF decreased (0.67 ± 0.04 preop and 0.57 ± 0.03 postop; P < 0.05). The mean EF did not change in the entire group (0.65 ± 0.02 preop and 0.64 ± 0.02 postop; P = NS). We conclude that patent coronary artery bypass grafts are associated with maintenance of myocardial function in patients with normal preop ventricular function. In patients with depressed ventricular performance, patent grafts result in improvement of regional and global function while occluded grafts result in depression of regional and global performance.THE RELIEF OF ANGINA PECTORIS after coronary artery bypass surgery is now well-documented.1-3 Although symptomatic improvement is a therapeutic goal, assessment of patient symptoms remains subjective, and there is poor correlation of symptoms with objective parameters of myocardial blood flow and ventricular performance in patients with coronary artery disease. The question of whether surgery ultimately improves patient longevity is currently under study. It is known that the state of left ventricular function is a potent predictor of patient survival for patients with coronary artery disease.4'5 Therefore, the effects of coronary bypass surgery upon left ventricular function may have impo...
Comparisons of the sensitivities of parameters for assessing left ventricular performance in man were made in 38 patients. The parameters compared were the ejection fraction, ventriculographic contraction patterns, the left ventricular end-diastolic pressure, and the contractile indices including the contractile element velocity at 10 mm Hg (Vce 10) and maximal contractile element velocity (Vmax). The contractile indices were obtained by catheter tip manometry, utilizing developed pressure (DP) to calculate the velocity of contractile element shortening (Vce) from the formula: dp/dt divided by 32 DP. Vce 10 was measured directly and Vmax was derived by linear manual extrapolation of the pressure-velocity plot to 0 mm Hg. Vmax values derived from linear manual extrapolation were compared with values obtained by computer least squares fitting of the Vce and developed pressure data points to single and double exponential equations. The Vce and developed pressure data points fit the single exponential equation better than the double exponential equation but the use of either equation resulted in slightly higher values for Vmax than obtained with linear manual extrapolation. The effect of heart rate on myocardial contractility was eliminated by making comparisons at both a basal and atrial paced rate of 100. Utilizing all methods, 24 patients were identified to have ventricular dysfunction. The contractile indices were significantly less sensitive than any other parameter (P smaller than 0.05) and identified seven patients while the left ventricular end-diastolic pressure, ejection fraction, and presence of asynergy identified 15, 15, and 12 patients, respectively. The use of a common atrial paced rate of 100 did not increase the sensitivity of the contractile indices. Since there was only partial overlapping between parameters in the identification of left ventricular dysfunction, the combination of different parameters was more sensitive than any single parameter alone. It is concluded that several methods are required to identify all patients with left ventricular dysfunction and that the contractile indices are the least sensitive indicator of left ventricular dysfunction.
Platelets have been implicated in the pathogenesis of coronary artery disease, and a number of studies have examined platelet function and coagulation parameters in such patients. We have examined platelet coagulant activities, volumes, and aggregate ratios in 23 patients with chest pain, seven of whom had normal coronary angiograms (group I) and 16 of whom had angiographically proven coronary artery disease (group II). There were no significant differences in the mean values for platelet volume or platelet aggregate ratios between the two groups. The platelet coagulant activities concerned with initiation and the early stages of intrinsic coagulation were significantly increased in patients in group II as compared with those in group I. No significant differences were noted between the two groups with respect to prothrombin time, partial thromboplastin time, and plasma levels of fibrinogen and coagulation factors V and VIII. However, the mean activity in plasma of antithrombin III (but not the level of antithrombin III antigen) was significantly lower in patients of group II compared with group I. Overall, our observations provide evidence for an enhanced contribution of platelets to the intrinsic coagulation system in patients with coronary artery disease. The platelet coagulant hyperactivity noted in these patients may reflect a role of platelets in the pathogenesis of coronary artery disease or may be secondary to the underlying arterial disease. Circulation 69, No. 1, 15-21, 1984. PLATELETS have been implicated in the pathogenesis of coronary artery disease, and a number of studies have been carried out to examine various aspects of platelet function in this disorder. These have included the study of platelet responses such as adhesion, aggregation, and the formation of vasoactive prostaglandin derivatives, the quantitation of platelet aggregate ratio and plasma levels of platelet-specific proteins (,Bthromboglobulin and platelet factor 4), and the estimation of the survival of platelets in patients with coro
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