Citations

A correlation of the clinical and electrocardiographic findings was undertaken in 110 cases which had in common the presence of deeply inverted T waves in central terminal leads centered about position 3 on the precordium. The results of this study are reviewed. A summary is presented of changes encountered at the time of necropsy in nine cases in which electrocardiographic changes of similar type had been recorded. These observations are integrated with concepts derived from the dipole theory. The total evidence is viewed in relation to observations reported by other investigators.

Previous studies in this series demonstrated structural changes in the pulmonary vascular bed as the result of mitral valvular disease and other cardiac disorders. The present study demonstrates changes in the lungs as the result of chronic left ventricular failure; these changes were like those produced by mitral stenosis. The most pronounced disturbance was medial hypertrophy. The exact mechanism is not known, but it probably is related to increased pulmonary venous pressure.

Evidence is presented which indicates that shunting of small amounts of blood from right to left occurs frequently through interatrial communications. Such right-to-left shunts are of small magnitude in the usual case of atrial septal defect, but it appears that of the fractions of blood shunted, a greater proportion has originated from the inferior vena cava than from the superior vena cava.

Fluorescent quantitation of epinephrine and norepinephrine in plasma of patients suspected of having pheochromocytomas is of considerable diagnostic value. The concentrations of these pressor amines in normal subjects, patients with various diseases with and without hypertension, and 13 patients with pheochromocytomas are reported. In all patients with pheochromocytomas and sustained hypertension the concentrations of pressor amines were significantly elevated. However, in patients with paroxysmal hypertension secondary to pheochromocytomas the pressor amine concentrations may be unelevated when the blood pressures are normal. In this latter group provocative tests with intravenous histamine are indicated to induce hypertension prior to quantitating pressor amines.

Thirty-three cases of enterococcal endocarditis encountered during the decade from January 1944 through December 1953 are reviewed. In vitro studies indicate that penicillin and streptomycin are the best antibiotic pair for bactericidal effect. Twelve of the last 14 patients were cured (86 per cent), 10 with combined therapy. The cure rate in enterococcal endocarditis now approximates that of endocarditis caused by penicillin-sensitive streptococci. A maximal number of cures is achieved by individualization of therapy. The daily dosage of penicillin and the duration of combined penicillin-streptomycin therapy should be guided by in vitro bactericidal tests employing the patient's strain of enterococcus.

Abstract —In this review, we examine the possibility that small increments in angiotensin II are responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. A low dose of angiotensin II (2 to 10 ng · kg −1 · min −1 , which does not elicit an immediate pressor response), when given for 7 to 30 days by continuous intravenous infusion, can increase mean arterial pressure by 30 to 40 mm Hg. This slow pressor response to angiotensin is accompanied by the stimulation of oxidative stress, as measured by a significant increase in levels of 8-iso-prostaglandin F 2α (F 2 -isoprostane). Superoxide radicals and nitric oxide can combine chemically to form peroxynitrite, which can then oxidize arachidonic acid to form F 2 -isoprostanes. F 2 -isoprostanes exert potent vasoconstrictor and antinatriuretic effects. Furthermore, angiotensin II can stimulate endothelin production, which also has been shown to stimulate oxidative stress. In this way, a reduction in the concentration of nitric oxide (which is quenched by superoxide) along with the formation of F 2 -isoprostanes and endothelin could potentiate the vasoconstrictor effects of angiotensin II. We hypothesize that these mechanisms, which underlie the development of the slow pressor response to angiotensin II, also participate in the production of hypertension when circulating angiotensin II levels appear normal, as occurs in many cases of essential and renovascular hypertension.

Abstract —According to the “epinephrine hypothesis,” circulating epinephrine taken up by sympathetic nerves is coreleased with norepinephrine during sympathetic stimulation and binding of coreleased epinephrine to presynaptic β-adrenoceptors augments exocytotic release of norepinephrine, contributing to high blood pressure. This study examined whether infusion of a physiologically active amount of epinephrine affects subsequent vascular responses and the estimated rate of entry of norepinephrine into regional venous plasma (norepinephrine spillover). Each of 3 experiments included intravenous infusion of 3 H-norepinephrine, measurements of forearm vascular resistance, and intra-arterial infusion of epinephrine (3 ng/min per deciliter forearm volume). In experiment 1, subjects underwent lower body negative pressure (LBNP−25 mm Hg) before and after intra-arterial epinephrine; in experiment 2, LBNP and intra-arterial yohimbine before and after intra-arterial epinephrine; and in experiment 3, intravenous nitroprusside before and after intra-arterial epinephrine. In all subjects, intra-arterial epinephrine produced ipsilateral pallor and decreased forearm vascular resistance. Ipsilateral venous epinephrine increased by 10-fold. Epinephrine did not affect forearm vasoconstrictor responses to LBNP or vasodilator responses to intra-arterial yohimbine or intravenous nitroprusside; did not affect venous norepinephrine levels or norepinephrine spillover during LBNP, yohimbine, LBNP during yohimbine, or nitroprusside; and did not increase venous epinephrine levels during any of these manipulations. Loading of forearm sympathetic terminals with epinephrine therefore does not augment subsequent neurogenic vasoconstriction or norepinephrine release in the human forearm in response to sympathetic stimulation. The findings are inconsistent with the epinephrine hypothesis.

Background —Patients with treated diabetes in the randomized-trial segment of the Bypass Angioplasty Revascularization Investigation (BARI) who were randomized to initial revascularization with PTCA had significantly worse 5-year survival than patients assigned to CABG. This treatment difference was not seen among diabetic patients eligible for BARI who opted to select their mode of revascularization. We hypothesized that differences in patient characteristics, assessed and unmeasured, together with the treatment selection in the registry, at least partially account for this discrepancy. Methods and Results —Among diabetics taking insulin or oral hypoglycemic drugs at entry, angiographic and clinical presentations were comparable between randomized and registry patients. However, more registry patients were white, and registry diabetics tended to be more educated and more physically active and to report better quality of life. Procedural characteristics and in-hospital complications were comparable. The 5-year all-cause mortality rate was 34.5% in randomized diabetic patients assigned to PTCA versus 19.4% in CABG patients ( P =0.0024; relative risk [RR]=1.87); corresponding cardiac mortality rates were 23.4% and 8.2%, respectively ( P =0.0002; RR=3.10). The CABG benefit was more apparent among patients requiring insulin. In the registry, all-cause mortality was 14.4% for PTCA versus 14.9% for CABG ( P =0.86, RR=1.10), with corresponding cardiac mortality rates of 7.5% and 6.0%, respectively ( P =0.73; RR=1.07). These RRs in the registry increased to 1.29 and 1.41, respectively, after adjustment for all known differences between treatment groups. Conclusions —BARI registry results are not inconsistent with the finding in the randomized trial that initial CABG is associated with better long-term survival than PTCA in treated diabetic patients with multivessel coronary disease suitable for either surgical or catheter-based revascularization.

Background —Surgical correction of mitral regurgitation in patients with no or mild symptoms remains controversial, particularly because the impact of preoperative symptoms on postoperative outcome is unknown. Methods and Results —The long-term outcome of 478 patients with organic mitral regurgitation (199 in NYHA functional class I/II and 279 in class III/IV before surgery) operated on between 1984 and 1991 was analyzed. In patients in NYHA class I/II before surgery compared with those in class III/IV, postoperative long-term survival was higher (at 10 years, 76±5% versus 48±4%, P <0.0001), with lower operative mortality (0.5% versus 5.4%, P =0.003) and better late survival ( P <0.0001). Comparison of observed and expected survival showed identical curves in patients in class I/II before surgery ( P =0.18), whereas excess mortality was observed in patients in class III/IV before surgery ( P <0.0001). Excess mortality associated with severe symptoms was also confirmed in all subgroups (all P <0.003) and in multivariate analysis ( P =0.0036; adjusted hazard ratio [95% CI], 1.81 [1.21 to 2.70]). Conclusions —In patients with organic mitral regurgitation, preoperative functional class III/IV symptoms are associated with excess short- and long-term postoperative mortality independently of all baseline characteristics. These data should lead to consideration of surgical correction of severe organic mitral regurgitation when no or minimal symptoms are present in patients at low operative risk, especially if repair is feasible.