To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.
SUMMARY In order to compare the venodilation effect of morphine in normal individuals (22) with that in patients (13) with heart failure morphine sulfate (0.1 mg/kg) was administered to 13 patients with mild pulmonary edema. After morphine congestive symptoms improved and venodilation was induced as determined by two independent techniques: venous pressure fell 10.2 mm Hg by the isolated hand technique and the venous volume of the forearm increased by 0.48 cc/100 ml, measured by the equilibration technique.ALTHOUGH MORPHINE has been used for years in the treatment of pulmonary edema, the mechanism by which it exerts its favorable effect is not completely understood. Animal studies suggest that morphine produces a significant venodilation and moves significant quantities of blood from the central to the peripheral circulation." 2 The term "'medical phlebotomy" has been coined to describe this phenomenon. In studies on normal human volunteers, however, the magnitude of the venodilation induced by morphine has been shown to be quite minimal, and the amount of blood that could be pooled in the limbs has been calculated to be quite small.' The effects of morphine on the peripheral venous system in patients with pulmonary edema might be quite different. These patients have an increased venous tone,4 which is at least in part related to increased activity of the sympathetic nervous system.7 Since the vasodilation induced by morphine in normal subjects has been shown to be secondary to a reduction in sympathetic nervous system activity, perhaps at the central nervous system level,4 it is reasonable to postulate that morphine might induce greater venodilation in patients with pulmonary edema. Our study shows that even though morphine does induce a greater reflex relaxation of the limb capacitance vessels than that demonstrated in normal volunteers, the effect is still too minor to explain the clinically beneficial results of morphine administration. MethodsPatients participating in this study were a highly selected group with acute pulmonary congestion who had been stabilized at least partially with the simple therapeutic measures of oxygen and bed rest. If a patient did not stabilize within 10 min, the patient was then given standard clinical treatment and the study was not performed. All 13 patients chosen for study still had rales over at least one-half of the posterior chest and were dyspneic in the seated posiNeither finding differed from those in normal individuals. Reflex venoconstriction noted on the taking of a single deep breath was unaffected by morphine administration and was similar to that observed in normal subjects. Since the drug morphine sulfate does not cause a major pooling of blood in the limbs, the favorable effect of narcotics in patients with pulmonary edema must be caused by other mechanisms such as splanchnic pooling, afterload reduction or reduced breathing effort. tion with oxygen. The etiology of their left heart failure was valvular (4), cardiomyopathic (3), and coronary (6) heart disease. ...
Left ventricular (LV) shape change during systole was characterized in nine patients with typical clinical findings of the systolic click syndrome (SCS) by means of cineangiographic measurements of three segmental diameters of the LV cavity and of the mitral valve ring (MVR) and contrasted with findings in eight patients with normal LV function. In the latter group, shortening of the proximal, midventricular, and apical segment diameters was comparable, averaging 38.6, 40.3, and 46.8%, respectively; MVR shortening averaged 31.8%. The velocity of fiber shortening, estimated as mean circumferential fiber shortening rate (mean FSR), was also similar in the three segments (1.66, 1.84, and 2.09 circ/sec). In patients with SCS, the extent of shortening and mean FSR in the proximal ventricular segment were consistently reduced (average 22.2%,P< 0.005; and 0.96 circ/sec,P< 0.025 respectively), and the MVR exhibited either reduced extent of contraction (four patients) or was unchanged or increased in diameter during systole (five patients). However, shortening of the midventricular and apical segments was normal, averaging 37.5 and 40.5%, respectively, as was the mean FSR in these segments (averages 1.60 and 1.70 circ/sec).These findings are consistent with a primary disorder of the myocardium in SCS localized to the inflow region of the left ventricle.
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