Measurement of right ventricular mass in normal and dilated cardiomyopathic ventricles using cine magnetic resonance imaging.

The accurate quantification of right ventricular (RV) mass has eluded conventional imaging modalities. Accordingly, cine magnetic resonance imaging was used for quantification of RV as well as left ventricular (LV) mass in 10 normal subjects and in 10 patients with dilated cardiomyopathy with an LV ejection fraction less than 0.40. Hearts were imaged with 10 mm thick short-axis slices from apex to base with a short echo delay time of 5 ms. Each slice was partitioned into 3 sections: RV free wall, ventricular septum and LV free wall, for calculation of end-diastolic and end-systolic mass and LV:RV free wall ratio. RV end-diastolic mass in normal subjects was 45 +/- 8 g, which was similar to the values determined in previously published postmortem studies, mean 46 g (range 23 to 68). The value determined in patients with dilated cardiomyopathy was higher (50 +/- 11 g), but this difference was not significant. LV:RV free wall ratio in cardiomyopathy (3.6 +/- 1.0) was greater than in normal subjects (2.4 +/- 0.3), because of the greater LV free wall mass in dilated cardiomyopathy, where LV free wall end-diastolic mass was 173 +/- 40 g vs 107.1 +/- 19.9 g in normal subjects (p less than 0.05). RV mass measurements had 6.4 +/- 3.6% interobserver and 7.3 +/- 6.1% intraobserver variability. There were no significant differences between end-diastolic and end-systolic mass measurements. Thus, cine magnetic resonance imaging can reproducibly calculate RV mass. The values in normal subjects correspond to previously reported postmortem values for a population without heart disease.

Application of cine nuclear magnetic resonance imaging for sequential evaluation of response to angiotensin-converting enzyme inhibitor therapy in dilated cardiomyopathy.

Cine nuclear magnetic resonance (NMR) imaging was used to serially measure cardiovascular function in 17 patients with New York Heart Association class II or III heart failure and left ventricular ejection fraction less than or equal to 45% who were treated for 3 months with benazepril hydrochloride, a new angiotensin-converting enzyme inhibitor, while continuing treatment with diuretic agents and digoxin. Interobserver reproducibilities for ejection fraction (r = 0.94, SEE 3.3%), end-systolic volume (r = 0.98, SEE 10.6 ml), end-diastolic volume (r = 0.99, SEE 8.29 ml), end-systolic mass (r = 0.96, SEE 15.4 g), end-systolic wall stress (r = 0.91, SEE 10 dynes.s.cm-5) and end-systolic stress/volume ratio (r = 0.85, SEE 0.13) demonstrated applicability of cine NMR imaging for the serial assessment of cardiovascular function in response to pharmacologic interventions in patients with heart failure. During 12 weeks of treatment with benazepril, ejection fraction increased progressively from 29.7 +/- 2.2% (mean +/- SEM) to 36 +/- 2.2% (p less than 0.05), end-diastolic volume decreased from 166 +/- 14 to 158 +/- 12 ml (p = NS), end-systolic volume decreased from 118 +/- 12 to 106 +/- 11 ml (p less than 0.05), left ventricular mass decreased from 235 +/- 13 to 220 +/- 12 g (p less than 0.05), end-systolic wall stress decreased 29% from 90 +/- 5 to 64 +/- 5 dynes.s.cm-5 (p less than 0.05), end-systolic pressure decreased from 92.6 +/- 3.7 to 78.8 +/- 5.3 (p less than 0.05) and end-systolic stress/volume ratio, a load-independent index of contractility, decreased from 0.83 +/- 0.05 to 0.67 +/- 0.06 (p less than 0.05), demonstrating that improved ejection fraction is due to afterload reduction.

Benefits of glucose and oxygen in multidose cold cardioplegia.

We tested the effects of glucose and oxygen in cardioplegic solutions on myocardial protection in the isolated perfused working rat heart. Recovery from 2 hours' hypothermic (8 degrees C) cardioplegic arrest was examined in 93 hearts. Cardioplegic solution, which was delivered every 15 minutes, was supplemented with glucose 28 mmol/L as a substrate or sucrose 28 mmol/L as a nonmetabolizable osmotic control; it was equilibrated with either 98% oxygen or 98% nitrogen, both with 2% carbon dioxide. Four combinations of hyperkalemic cardioplegic solution were studied: nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose. During hypothermic arrest, oxygenation of cardioplegic solution greatly reduced myocardial lactate production and prevented ischemic contracture as indicated by coronary vascular resistance. Glucose increased lactate production modestly but significantly only when the cardioplegic solution was nitrogenated. Although end-arrest myocardial adenosine triphosphate and creatine phosphate were greatly increased by oxygenation of cardioplegic solution (p less than 0.005), we could not detect improved preservation of these high-energy phosphates by glucose. Averaged over reperfusion, percent recovery of cardiac output for the nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose solutions was 32.3% +/- 6.1%, 45.9% +/- 4.6%, 44.5% +/- 4.6%, and 62.2% +/- 4.5%, respectively. Oxygenation of the glucose solution or addition of glucose to the oxygenated solution significantly improved recovery of cardiac output. The benefits of glucose and oxygen were additive, so that the oxygen-glucose cardioplegic solution provided the best functional recovery. We conclude that the addition of glucose to the fully oxygenated multidose cold cardioplegic solution improves functional recovery without increasing lactate production during arrest.

Oxygenated cardioplegia: the metabolic and functional effects of glucose and insulin.

Reports differ as to the efficacy of glucose and insulin as cardioplegic additives. Although deliberate oxygenation of crystalloid cardioplegic solutions improves myocardial protection, little is known about the protection afforded by glucose and insulin in such oxygenated solutions. In the isolated working rat heart, we studied the addition of oxygen, glucose, and insulin, separately and together, to a cardioplegic solution. The solution was equilibrated with O2 or N2, with glucose added as a substrate or sucrose as a nonmetabolizable osmotic control, with or without insulin. Hearts were arrested for 2 hours at 8 degrees C by multidose infusions. Oxygenation decreased lactate production and improved high-energy phosphate and glycogen preservation during arrest, prevented ischemic contracture, and improved functional recovery. The addition of glucose to the oxygenated solution increased the level of adenosine triphosphate at end-arrest from 10.5 +/- 0.5 to 13.9 +/- 0.6 nmol/mg dry weight and glycogen stores from 18.7 +/- 2.5 to 35.7 +/- 5.5 nmol/mg dry weight. The further addition of insulin did not better preserve these metabolites. Improvements in functional recovery due to glucose or insulin in the oxygenated solution attained statistical significance when both additives were included. Glucose increased lactate production significantly only when the solution was nitrogenated. Insulin added to the nitrogenated glucose-containing solution increased adenosine triphosphate and glycogen levels after 1 hour of arrest; and, although insulin did not prevent ischemic contracture from developing during the latter part of arrest with profound depletion of these metabolites, functional recovery was improved. The mechanism of improved functional recovery by insulin is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial oxygen use during epinephrine administration to ischemically injured canine hearts.

The rationale for inotropic support by epinephrine during cardiac surgery and the early postoperative period was examined in 11 dogs after 20 minutes of normothermic ischemia and 1 hour of reperfusion. Ischemia reduced myocardial adenosine 5'-triphosphate (ATP) content by 37%. Left ventricular performance was assessed from pressure-dimension loops generated by minor-axis-diameter crystals for a range of controlled loading as high as end-diastolic pressures of 15 mm Hg. Myocardial oxygen consumption was determined at 6-9 steady-state steps throughout this range, including those at basal conditions of the empty beating ventricle. The hearts were artificially paced at 160 beats/min. Higher oxygen consumption with epinephrine (0.5 microgram/min/kg) administration was demonstrated at all levels of left ventricular performance and at all end-diastolic lengths. Several mechanisms for higher oxygen cost for similar external work performances have been suggested. From this study, it appears that increased uptake of free fatty acids, which increased threefold during epinephrine infusion, contributes to less efficient use of oxygen for mechanical work. We conclude that the use of inotropic support in ischemically injured hearts for reasons other than overt heart failure is not well based because myocardial oxygen consumption increases even when greater work is performed at lower end-diastolic dimensions.

Myocardial reperfusion injury. Role of myocardial hypoxanthine and xanthine in free radical-mediated reperfusion injury.

The aim of this study was to differentiate myocardial reperfusion injury from that of ischemia. We assessed the role of the myocardial adenosine 5'-triphosphate (ATP) catabolites, hypoxanthine and xanthine, generated during ischemia and the early phase of reperfusion, in reperfusion injury by modulating adenosine transport and metabolism with specific metabolic inhibitors. This was followed by intracoronary infusion of exogenous hypoxanthine and xanthine. Twenty-four dogs instrumented with minor-axis piezoelectric crystals and intraventricular pressure transducers were subjected to 30 minutes of normothermic global myocardial ischemia and 60 minutes of reperfusion. In Group 1 (n = 7), normal saline was infused into the cardiopulmonary bypass reservior before ischemia and before reperfusion. Saline solution containing 25 microM p-nitrobenzylthioinosine (NBMPR) and 100 microM erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) was infused in Group 2 (n = 10) dogs. Group 3 (n = 7) dogs were treated exactly like those in Group 2 except, at the end of the ischemic period and immediately before releasing the cross-clamp, a solution of EHNA-NBMPR containing 100 microM hypoxanthine and 100 microM xanthine was infused into the aortic root. Left ventricular performance and myocardial adenine nucleotide pool intermediates were determined before and after ischemia. ATP was depleted by about 50% (p less than 0.05 vs. preischemia) in all groups after 30 minutes of ischemia. Inosine was the major ATP catabolite (9.29 +/- 1.2 nmol/mg protein) in Group 1, while adenosine (9.91 +/- 0.7 nmol/mg protein) was the major metabolite in EHNA-NBMPR-treated dogs (Groups 2 and 3). Hypoxanthine levels were fivefold more in Group 1 compared with Groups 2 and 3 (p less than 0.05). Left ventricular performance in Group 1 decreased from 76.8 +/- 7.6 to 42.9 +/- 9.8 and 52.3 +/- 8.4 dynes/cm2 x 10(3) (p less than 0.05), while myocardial ATP decreased from 30.9 +/- 2.2 to 17.2 +/- 1.0 and 16.5 +/- 1.0 nmol/mg protein during 30 and 60 minutes of reperfusion, respectively (p less than 0.05 vs. preischemia). Ventricular function in Group 2 dogs completely recovered within 30 minutes of reperfusion, and myocardial ATP recovered to the preischemic level at 60 minutes of reperfusion. In Group 3, left ventricular performance was depressed by 39% and 30% during 30 and 60 minutes of reperfusion (p less than 0.05), respectively, and myocardial ATP did not recover during reperfusion despite a significant intramyocardial adenosine accumulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiovascular manifestations of systemic lupus erythematosus.

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.

The response of neonates to intra-uterine sounds.

Playing prerecorded intra-uterine sounds to newborns reportedly soothes the babies. This study investigates this claim, particularly because of its promise for identifying neonates with severe hearing losses. 60 babies, up to eight days old, were observed individually under two conditions. In one, activity was rated on the Brazelton scale before and during presentation of intra-uterine sounds. In another, similar ratings were made but no sounds presented. The results indicate that intra-uterine sounds calm 90 per cent of babies who are fussy or crying but have no evident effect on babies who are awake but merely alert or who are slightly drowsy. These findings are discussed and improvements in procedure are suggested for use of intra-uterine sounds in routine screening for severe neonatal hearing loss.