Cigarette and waterpipe smoking associated knowledge and behaviour among medical students in Lebanon.

As future physicians capable of controlling tobacco dependence in the population, medical students are considered a main target for tobacco control interventions. This cross-sectional study reported on the prevalence of tobacco use (cigarettes and waterpipes) and associated knowledge and behaviour among 6th-year medical students in 2009-2010 from 6 medical schools in Lebanon. The self-administered questionnaire based on the Global Health Professional Survey (GHPSS) core questions also enquired about training in tobacco cessation approaches. All enrolled students were asked to participate; the response rate was 191/354 (54.3%). The prevalence of tobacco use was 26.3% for cigarettes and 29.5% for waterpipes. Smoking waterpipes was the only significant predictor for cigarette smoking and there was no difference by sex and socioeconomic status. A minority reported ever receiving any formal training in treatment approaches for tobacco dependence. Medical schools should include tobacco dependence treatment training programmes in their curriculum and discourage tobacco use.

Prevention of bedrest-induced physical deconditioning by daily dobutamine infusions. Implications for drug-induced physical conditioning.

The effects of intermittent infusions of dobutamine were studied in young normal male subjects during a period of bedrest deconditioning to determine whether this synthetic catechol affects physical conditioning processes in humans. 24 volunteers were placed at bedrest and randomized to daily 2-h treatments of saline infusions (control), dobutamine infusions, or maintenance exercise (control). Exercise, hemodynamic, and metabolic studies were performed at base line and at the termination of the 3-wk treatment period. Maximal exercise (duration, oxygen consumption, and workload) fell for the saline group and remained unchanged for the dobutamine and exercise groups. Hemodynamics during exercise were maintained the same as pretreatment base line for the dobutamine and exercise groups, whereas stroke volume and cardiac output dropped and heart rate rose for the saline group. The metabolic profile showed an increased blood lactate response at rest and during submaximal exercise after 3 wk of bedrest for the saline group, and essentially no change for the exercise and the dobutamine groups. Extraction of oxygen across the exercising lower limb rose for the dobutamine group, as did the activity of the skeletal muscle oxidative enzymes, citrate synthetase, and succinate dehydrogenase. In contrast to the exercise control group, the saline and dobutamine groups developed orthostatic hypotension, tachycardia, and accentuation of the renin-aldosterone response over the 3-wk treatment period; for the saline group, this is best explained by the observed fall in blood volume and for the dobutamine group, by the blunting of vascular vasoconstrictive responses. During a period of bedrest deconditioning in humans, infusions of dobutamine maintain many of the physiologic expressions of physical conditioning.

Long-term indoramin therapy in congestive heart failure: a double-blind, randomized, parallel placebo-controlled trial.

Twenty-one patients with moderately severe congestive heart failure participated in a double-blind, randomized, parallel placebo-controlled trial designed to evaluate the effects of long-term (2 months) indoramin therapy on rest and exercise hemodynamics, exercise capacity and clinical status of patients with this clinical syndrome. The long-term administration of indoramin in patients (mean dose 50 mg every 12 hours) caused a mild reduction from baseline values in supine rest mean systemic blood pressure and, after dosing, elicited a significant reduction in systemic and pulmonary vascular resistances, pulmonary capillary wedge pressure and heart rate as well as a mild increase in stroke volume. Long-term indoramin therapy caused a small decrease, as compared with baseline exercise responses, in systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure at submaximal levels of exercise. It did not alter hemodynamic variables at maximal exercise, exercise capacity or overall clinical status, compared with findings at baseline or with placebo.

In vivo validation of the origin of the esophageal electrocardiogram.

Esophageal electrocardiography is a clinical and investigational technique that is useful for determining atrial conduction intervals, analyzing atrial rhythms and mapping conduction pathways. Although the left atrial origin of the esophageal electrocardiogram has long been implied, recently that origin has been questioned. In the present study, the origin of the esophageal deflection is defined by direct right and left atrial mapping studies performed with simultaneous esophageal electrograms obtained from three positions (high, mid and low). Seven patients with normal left atrial dimensions (group I) and five patients with left atrial enlargement (group II) underwent transseptal catheterization during the course of electrophysiologic study. In group I (normal left atrial dimensions), conduction time from the high right atrium to each of the three esophageal positions corresponded to conduction times to left atrial sites ranging from 1 to 3 cm lateral to the left interatrial septum. The mid- and low esophageal conduction times were all significantly longer than conduction time to the left side of the septum (p less than 0.05). In group II (enlarged left atrium), conduction times to each of the esophageal sites corresponded to conduction times to left atrial sites lying between the mid-left atrium and a point 1 cm lateral to the left side of the septum. A significant trend toward longer conduction time to the mid-esophageal position than to the left septum was noted (p less than 0.1). In both groups, conduction times measured with the esophageal catheter were significantly longer than conduction time to the right interatrial septum (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Parasympathetic withdrawal is an integral component of autonomic imbalance in congestive heart failure: demonstration in human subjects and verification in a paced canine model of ventricular failure.

Although enhanced sympathetic tone is a well recognized component of the autonomic profile characteristic of congestive heart failure, the contribution of parasympathetic withdrawal to this autonomic imbalance is less well described. The technique of spectral analysis of heart rate variability provides a dynamic map of sympathetic and parasympathetic tone and was thus used to define the nature of sympathetic-parasympathetic interactions in humans with idiopathic dilated cardiomyopathy and in a paced canine model of congestive heart failure. Humans with cardiomyopathy were found to have an augmentation of the sympathetically mediated low frequency area of the power density spectrum. Parasympathetic withdrawal was demonstrated by significant reductions in the parasympathetically mediated high frequency area (p less than 0.05) and the ratio of high to low frequency areas (p less than 0.01). Administration of atropine to normal subjects resulted in a significant reduction in the high frequency area (p less than 0.05) and the high/low frequency area ratio, both of which decreased within the range noted in patients with congestive heart failure. Administration of isoproterenol in normal subjects led to an augmentation of the low frequency area but to only a small decrease in the high/low frequency area ratio. Induction of congestive heart failure in a paced canine model resulted in alterations in the autonomic profile that resembled those seen in humans with ventricular failure. The prominent high frequency region of the spectrum at baseline, indicating a predominance of parasympathetic tone, was absent after the evolution of congestive heart failure, and there was a marked augmentation of the low frequency region of the spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative investigation of cardiomyocyte hypertrophy and myocardial fibrosis over 6 years after cardiac transplantation.

OBJECTIVES: This study was performed to determine the degree and time course over 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the cardiac allograft in transplanted patients. BACKGROUND: Diastolic dysfunction and to a certain extent systolic dysfunction are common cardiac findings after heart transplantation. The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely contributes to these derangements. METHODS: Cardiomyocyte diameter and percent fibrosis were determined in serial endomyocardial biopsy specimens obtained from 1 month up to 6 years following heart transplantation in 50 patients. Endomyocardial biopsy specimens from 40 patients with primary dilated cardiomyopathy and 11 normal subjects were similarly analyzed for control data. Analyses were performed in a blinded format using a validated computerized image analysis system (Optimas 5.2). RESULTS: Early (1 month) cardiomyocyte enlargement decreased to the smallest diameter 6 months posttransplant, but thereafter progressively increased by 10% to 20% over the subsequent 5- to 6-year period. Although not statistically established, principal stimuli may include a discrepancy in body size (recipient > donor), coronary allograft vasculopathy and posttransplant systemic hypertension. Percent myocardial fibrosis rose early (1 to 2 months) posttransplant and thereafter remained at the same modest level of severity. CONCLUSIONS: Cardiomyocyte diameter of the transplanted heart gradually increases over time, while percent myocardial fibrosis rises early and remains in a modestly elevated plateau after 2 months posttransplant. These histostructural changes likely contribute to the hemodynamic and cardiac functional alterations commonly observed posttransplant.

Influence of positive inotropic therapy on pulsatile hydraulic load and ventricular-vascular coupling in congestive heart failure.

The aortic input impedance spectrum provides a description of the total hydraulic load imposed on the left ventricle and may be used to assess the coupling of the ventricle to the vasculature. The adaptation of the vasculature to positive inotropic intervention was examined in 10 patients with idiopathic dilated cardiomyopathy to test the hypothesis that increased myocardial contractility is matched by complementary changes in aortic impedance that optimize ventricular-vascular coupling and maximize power transfer to the circulation. High fidelity intravascular recordings of aortic pressure and flow were obtained at baseline study and during infusion of dobutamine to derive the aortic input impedance spectrum. In eight patients in whom increased staged infusion of dobutamine resulted in a significant increase in stroke volume (22.3 +/- 14.5 ml/beat increase over baseline), the significant (p less than 0.05) increase in the maximum of the first derivative left ventricular pressure pulse (dP/dt) was accompanied by significant decreases in characteristic impedance of the aorta (138 +/- 88 to 92 +/- 44 dyne.s.cm-5) wave reflection index (238 +/- 144 to 109 +/- 59 dyne.s.cm-5), and low frequency moduli of impedance. Effective positive inotropic therapy with dobutamine in the setting of congestive heart failure is accompanied by complementary changes in the aortic impedance spectrum, which represent a matching of impedance to the increased contractile state of the ventricle and facilitation of ventricular-vascular coupling.

Plasma atherogenic markers in congestive heart failure and posttransplant (heart) patients.

OBJECTIVES: We hypothesized that plasma factors important for the development of atherosclerosis play a major role in the occurrence of cardiac allograft vasculopathy (CAV). BACKGROUND: Cardiac allograft vasculopathy is a major cause of death among heart transplant recipients, has a poorly understood pathogenesis and has similarities to atherosclerotic coronary disease. METHODS: The study population consisted of 93 postcardiac transplant recipients. Thirty-one patients with congestive heart failure (CHF) and 18 healthy individuals served as control subjects. Posttransplant coronary anatomy was evaluated by angiography and intravascular ultrasound. Laboratory analyses of lipids, homocysteine, vitamin B12 and folate, fibrinogen, von Willebrand factor antigen (vWFAg) and renin were obtained on all participants. RESULTS: Posttransplant patients were found to have elevated serum triglycerides, total cholesterol/ high-density lipoprotein cholesterol ratio, lipoprotein (a), homocysteine, vWFAg, fibrinogen and renin and lower high-density lipoprotein cholesterol. Most of these laboratory atherogenic factors were also elevated to a similar degree in the CHF control population. Although most atherogenic markers were elevated, there was little correlation with CAV severity. Cardiac allograft vasculopathy severity varied with time after transplantation, 3-hydroxy-methyl-glutaryl-coenzyme A reductase inhibitor use and prior cytomegalovirus infection. Even within the normal range, lower RBC folate levels were associated with increased severity of CAV. CONCLUSIONS: The posttransplant course is associated with increased clinical and laboratory atherogenic factors, some of which likely contribute to the severity of coronary vasculopathy. Compared with normal control subjects, many of these markers are already increased in pretransplant CHF patients with or without occlusive coronary artery disease.

Sustained augmentation of parasympathetic tone with angiotensin-converting enzyme inhibition in patients with congestive heart failure.

OBJECTIVES: The objective of this investigation was to evaluate the changes in parasympathetic tone associated with long-term angiotensin-converting enzyme inhibitor therapy in patients with congestive heart failure. BACKGROUND: Angiotensin-converting enzyme inhibitors provide hemodynamic and symptomatic benefit and are associated with improved survival in patients with congestive heart failure. Angiotensin II, whose production is ultimately inhibited by these agents, exerts significant regulatory influence on a variety of target organs including the central and peripheral nervous systems. Accordingly, it would be anticipated that angiotensin-converting enzyme inhibitors would significantly alter the autonomic imbalance characteristic of patients with congestive heart failure and that this influence over neural mechanisms of cardiovascular control may significantly contribute to the hemodynamic benefit and improved survival associated with angiotensin-converting enzyme inhibitor therapy. METHODS: In the current investigation, changes in autonomic tone associated with long-term administration of an angiotensin-converting enzyme inhibitor were measured using spectral analysis of heart rate variability in 13 patients with congestive heart failure who were enrolled in a double-blind randomized placebo-controlled trial of the angiotensin-converting enzyme inhibitor zofenopril. Both placebo and treatment groups were balanced at baseline study in terms of functional class, ventricular performance and autonomic tone. RESULTS: After 12 weeks of therapy with placebo, there was no change in total heart rate variability, parasympathetically governed high frequency heart rate variability or sympathetically influenced low frequency heart rate variability. In contrast, therapy with zofenopril was associated with a 50% increase in total heart rate variability (p = 0.09) and a significant (p = 0.03) twofold increase in high frequency heart rate variability, indicating a significant augmentation of parasympathetic tone. CONCLUSIONS: These results demonstrate that long-term treatment of patients having congestive heart failure with an angiotensin-converting enzyme inhibitor is associated with a restoration of autonomic balance, which derives in part from a sustained augmentation of parasympathetic tone. Such augmentation of vagal tone is known to be protective against malignant ventricular arrhythmias in patients with ischemic heart disease and therefore may have similar benefit in the setting of ventricular failure, thus contributing to the improved survival associated with angiotensin-converting enzyme inhibitor therapy in patients with congestive heart failure.

Clinical pharmacology of nicorandil in patients with congestive heart failure.

Nicorandil is a nicotinamide derivative with a potential role in human therapeutics because of its potent vasodilating properties. The pharmacokinetics of oral nicorandil administration and the relationships between plasma nicorandil concentration and hemodynamic responses were examined in 25 patients with moderate to severe congestive heart failure. The dose range from 10 to 60 mg was studied. Elimination half-life for this dose range was substantially longer than that previously reported in normal volunteers. Total area under the curve increased in a curvilinear fashion with progressive dose increments, indicating a disproportionate increase in systemically available drug at higher doses. Hemodynamic responses generally correlated well with plasma nicorandil concentration, with rapid loss of cardiovascular activity corresponding to the efficient clearance of nicorandil.

Histologic compaison of allograft myocardium between short- and long-term survivors of human cardiac transplantation.

Myocardial histology of cardiac allografts differed between short-term (<5 years) and long-term (>5 years) survivors after transplantation. These differences may partially be attributable to a higher prevalence of systemic hypertension and allograft rejection in the short-term survivors, affecting hemodynamics and allograft function.

The equilibrium position of the mitral valve: an accurate model of mitral valve motion in humans.

A "semiopen" diastolic equilibrium position of the mitral valve that is assumed in the absence of transmitral flow has been demonstrated in instrumented dogs. It has been suggested that the papillary muscles and chordae tendineae play an integral role in returning the valve to this position after initial diastolic opening. To determine whether such a model of mitral valve motion is valid in noninstrumented humans without underlying valvular disease, M-mode and Doppler ultrasound studies were performed in 6 subjects who underwent prolonged periods of ventricular diastole and atrial inactivity. After maximal opening, the mitral valve assumed a stable open position in which mean separation of the anterior and posterior mitral leaflets was 52% of maximal separation. This position was maintained for a mean duration of 585 ms, during which time transmitral flow fell to 0 m/s. Peak mitral valve opening preceded the early transmitral flow peak by an average of 42 ms, suggesting an active closure of the mitral valve as flow continued to accelerate. It is concluded that a semiopen equilibrium position of the mitral valve is assumed during prolonged diastolic periods in the absence of transmitral flow and is an accurate model describing diastolic mitral valve motion in noninstrumented humans. The chordae tendineae and papillary muscles may actively participate in the genesis and maintenance of the equilibrium position.

Cardiovascular pharmacology of dopexamine in low output congestive heart failure.

Dose-response infusions (0.25 to 4.0 micrograms/kg/min) and extended infusions of dopexamine, a new synthetic catechol with beta 2 adrenergic and dopaminergic agonist effects, were performed in 12 patients with low output congestive heart failure (CHF). The central and regional hemodynamic effects and responses in renal function were determined and compared with those of saline-placebo control patients in a randomized, double-blind, crossover design. Dopexamine significantly increased cardiac output at a dose greater than or equal to 0.25 micrograms/kg/min secondary to an increase in stroke volume at greater than or equal to 0.25 micrograms/kg/min and heart rate at greater than or equal to 0.50 micrograms/kg/min. Dopexamine evoked a significant decrease in systemic and pulmonary vascular resistances, with mild reductions noted for systemic and pulmonary diastolic pressures. Right and left ventricular filling pressures decreased over the entire dose range of dopexamine concomitant with a demonstrable improvement in the indexes of ventricular performance. Dopexamine preferentially increased visceral (renal, hepatic-splanchnic) blood flow over that of limb. Urine volume and sodium excretion increased slightly with dopexamine. Dopexamine elicits rather prominent vasodilating effects (particularly of visceral vascular beds), some positive inotropy and chronotropy and favorable responses in renal function.

Central and regional hemodynamic effects of flosequinan for congestive heart failure.

The central and regional hemodynamic effects of flosequinan, a new orally administered vasodilator, were examined in 10 patients with moderate to severe congestive heart failure. A single-blind design was used to compare a standard dose of flosequinan (100 mg) with placebo. Flosequinan produced a statistically significant increase in cardiac output, primarily through its augmentation of stroke volume. This response was accompanied by significant reductions in systemic vascular resistances and right and left ventricular filling pressures. A reduction in pulmonary artery pressure and total pulmonary vascular resistance also was observed. The vasodilatory actions of flosequinan improved overall left ventricular performance; the inotropic indexes measured were not altered. There were no significant changes in upper limb, renal or hepatic-splanchnic blood flow or in the vascular resistances of these regions after flosequinan administration. The upper limb venous capacitance increased significantly. First-dose flosequinan evokes favorable central hemodynamic changes and improves overall left ventricular performance in patients with congestive heart failure. The acute augmentation in cardiac output, however, is not accompanied by a preferential alteration of flow to any of the major vascular regions studied.

Effects of successful cardiac transplantation on plasma endothelin.

After cardiac transplantation, cyclosporine-treated patients exhibit a high incidence of systemic hypertension, the mechanism of which is not known. Endothelin, a potent vasoconstrictor peptide of endothelial origin, may be activated by cyclosporine-induced endothelial injury and therefore may mediate post-transplant hypertension. In the present study, we tested whether immunoreactive endothelin-1 could be detected by radioimmunoassay in the plasma of cardiac transplant recipients and if levels correlated with hemodynamic characteristics, cyclosporine level, or renal function as assessed by serum creatinine. Plasma endothelin was measured in 22 stable cyclosporine-treated patients 9 days to 3 years after successful orthotopic cardiac transplantation before routine hemodynamic assessment and surveillance endomyocardial biopsy. Fifteen patients were receiving chronic therapy for hypertension. Plasma endothelin-1 was 5.2 +/- 1.8 pg/ml (range 3.1 to 10.5), which was increased compared with that in 12 normal subjects (1.9 +/- 0.3 pg/ml; range 1.4 to 2.4); the difference was statistically significant (p < 0.0001). Repeated sampling in 8 patients at weekly intervals identified a persistent increase in endothelin with only modest variability. Endothelin-1 did not correlate with any hemodynamic variable, serum creatinine or cyclosporine level. Thus, endothelin-1 is increased after successful orthotopic cardiac transplantation. In the absence of discrete correlations with hemodynamic variables, serum creatinine or cyclosporine levels, both the characteristics and mechanisms for increased endothelin in recipients of cardiac transplants require further evaluation.

Hemodynamic effects of oral nicorandil in congestive heart failure.

Twenty-five patients with congestive heart failure (CHF) underwent a double-blind randomized study of the acute hemodynamic effects of orally administered nicorandil, a newly developed vasodilator drug. A dose range of 10 to 60 mg was studied. Nicorandil, at a dose of 60 mg, caused statistically significant decreases in systemic systolic and diastolic blood pressure, right atrial pressure, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance and systolic and diastolic pulmonary arterial pressure. A brief increase in cardiac index attributable to an increase in stroke volume without a change in heart rate was also observed. A dose of 40 mg produced similar results in cardiac index and systemic and pulmonary vascular resistance, but changes in other hemodynamic parameters were much smaller in magnitude and usually not of statistical significance. No significant hemodynamic response was seen to doses of 10 and 20 mg of nicorandil. Duration of action was short with nearly all hemodynamic parameters returning close to baseline within 3 hours. This rapid decrease in activity occurred in concert with a rapid plasma clearance of nicorandil as determined by serial measurements of plasma drug concentration. This study suggests that first-dose orally administered nicorandil elicits favorable, but brief, hemodynamic effects in CHF at doses greater than or equal to 40 mg.

Echocardiographic evaluation of pulmonary artery distensibility.

The aim of this study was to verify the hypothesis that pulmonary artery (PA) distensibility may modify the pattern of right ventricular ejection. Pulmonary artery distensibility was evaluated with M-mode measurements of right pulmonary artery diameter from suprasternal notch simultaneous with pulmonary pressure measurements. Pulmonary artery pressure was measured in 19 subjects, 29 to 75 years old (mean age, 49 years). Pulmonary artery systolic pressure was 22 to 108 mm Hg (mean, 52 mm Hg). Pulmonary artery pressure strain modulus (Ep) was calculated as follows: PADD x (PASP-PADP)/PADD-PADS (PADS-PA diameter in systole, PADD-PA diameter in diastole, PASP-PA systolic pressure, PADP-PA diastolic pressure) was 6 +/- 8 10(5) dynes/cm2. Right ventricular outflow tract velocity was recorded with pulsed Doppler echocardiography and acceleration times (AT) and ejection times (ET) were measured. Log Ep was correlated with pulmonary artery systolic and mean pressure (r = 0.90 and r = 0.87, p < 0.0001) but not with age (r = 0.30, p = NS). Acceleration time and AT/ET ratio were correlated with log Ep (r = 0.73 and r = 0.76, p < 0.001) and with pulmonary artery mean pressure (r = 0.91 and r = 0.89, p < 0.0001). When pulmonary artery pressure was included in multiple analyses, the relationships between Doppler indices and elastic modulus did not prove to be significant. These findings emphasize the independence of Doppler right ventricular outflow tract velocity indexes used for noninvasive evaluation of pulmonary hypertension from pulmonary artery distensibility in a clinical setting.

Thermodilution measures of right ventricular ejection fraction and volumes in heart transplant recipients: a comparison with radionuclide angiography.

A reliable, convenient measure of right ventricular ejection fraction may be a useful adjunct to evaluate cardiac allograft rejection. The purpose of this investigation was to compare two measures of right ventricular ejection fraction: (1) radionuclide angiography with the first-pass technique and (2) thermodilution with a balloon flotation catheter. The study was performed in 26 heart transplant recipients; hemodynamics, thermodilution cardiac output, and right ventricular ejection fraction were measured. First pass radionuclide angiography was performed either simultaneously (n = 11) or within 4 hours (n = 15) of the thermodilution study. Mean thermodilution right ventricular ejection fraction was 39% +/- 8%, and radionuclide angiography ejection fraction was 47% +/- 9%, which represents a highly significant difference (p < 0.001) in techniques. Linear regression showed no correlation between the two techniques (r = 0.3; p = NS). No differences in results were observed in those studied simultaneously versus less than 4 hours. We conclude that the thermodilution technique underestimates right ventricular ejection fraction in heart transplant recipients and that its usefulness as a tool to screen for systolic dysfunction related to rejection is limited.

Prospective study of the circadian pattern of blood pressure after heart transplantation.

BACKGROUND: Previous reports indicate that heart transplant recipients lack a normal nocturnal decline in blood pressure. This prospective study was designed to determine the evolution of circadian blood pressure patterns after heart transplantation. METHODS: Twenty-four-hour ambulatory blood pressure and heart rate was measured in eight heart transplant recipients early (47 +/- 35 days) and late (740 +/- 10 days) after transplantation. RESULTS: Early transplant recordings and the normal control group recordings showed similar daytime systolic blood pressure but had different nighttime systolic blood pressure (138 +/- 15 mm Hg versus 112 +/- 9 mm Hg, p = 0.0002). The percent nocturnal change in systolic blood pressure showed a nocturnal increase in blood pressure in the early recordings versus a decrease in the healthy subjects (+4 +/- 2.7 versus -13 +/- 5.4, p < 0.0001). The late recordings showed a significant decrease in the nighttime systolic blood pressure (138 +/- 15 mm Hg versus 119 +/- 7 mm Hg, p = 0.011). The percent nocturnal change in systolic blood pressure was also significantly different between the early and late recordings (+4 +/- 2.7 versus -9 +/- 9, p = 0.0082) indicating a return of a nocturnal decline in systolic blood pressure. Similar patterns in diastolic blood pressure were observed. No significant change in the percent nocturnal change in heart rate occurred (-10 +/- 4.1 versus -7 +/- 5.5). CONCLUSIONS: Prospective follow-up of this heart transplant population showed that diurnal blood pressure variation is restored in some patients; diurnal variation is not related to corticosteroids, cyclosporine, or heart rate.

Adenine nucleotide content in cold preserved human donor hearts and subsequent cardiac performance after orthotopic heart transplantation.

Myocardial high-energy phosphate content has been used as a parameter to evaluate the adequacy of donor organ preservation. The purpose of this study was to assess current techniques of preservation by measuring high-energy phosphates in cold preserved (4 degrees C) human donor hearts. Endomyocardial biopsy samples of the donor heart right ventricular septum (n = 24) were compared with samples from patients with normal cardiac function evaluated before chemotherapy (n = 12). Left ventricular and right ventricular ejection fractions were measured by means of radionuclide angiography early (24 to 72 hours) and late (mean 42 days) postoperatively. Mean total cold ischemic time was 146 +/- 54 minutes (range, 89 to 340 minutes). ATP nmol/mg noncollagenous protein in donor hearts was 38.2 +/- 10.7 and 31.9 +/- 13.6 (p = NS) in normal hearts. Early postoperative left ventricular and right ventricular ejection fraction was 55% +/- 14% and 40% +/- 9%, respectively. Late postoperative left ventricular and right ventricular ejection fraction was 64% +/- 14% and 50% +/- 10%, respectively; both represent significant increases in right and left ventricular ejection fraction (p less than 0.05). No correlation was found between ischemic time and donor ATP, ischemic time and ejection fraction, or ejection fraction and ATP. Three patients with normal donor heart ATP content had severe, but reversible, early graft dysfunction. In summary, currently used human donor heart preservation techniques are associated with normal values of high-energy phosphates and usually excellent early and late postoperative graft function.(ABSTRACT TRUNCATED AT 250 WORDS)