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PubMed1995

Exercise testing in pediatric heart, heart-lung, and lung transplant recipients.

Cardiorespiratory responses to progressive exercise were examined in 38 children who had undergone heart (n = 16), heart-lung (n = 13), or double-lung (n = 9) transplantation, and in 41 healthy controls. The four groups were similar in age, but the control subjects and heart transplant recipients were significantly larger than the heart-lung and lung recipients as assessed by body mass index (BMI). Time since transplant was significantly longer in the heart (601 days) compared with heart-lung (146 days) and lung (125 days) transplant groups. Physical work capacity and peak oxygen uptake were significantly reduced (43 to 64% of predicted) in the three transplant groups compared with the control group. Peak heart rate (percent predicted) was significantly higher in the control subjects (94%) compared with the heart (66%), heart-lung (70%), and lung (77%) transplant recipients. Peak minute ventilation was significantly higher in the control (72.9 L/min) and heart transplant (51.0 L/min) groups than the heart-lung (37.4 L/min) and lung (41.3 L/min) transplant groups. The control group had a higher peak tidal volume than the three transplant groups, and a higher peak respiratory rate than the lung transplant recipients. Correlational analysis revealed that physical work capacity (PWC) was significantly related to heart rate at peak exercise (HRpeak) and minute ventilation at peak exercise (VE-peak) in the heart transplant recipients, BMI, VEpeak, and FEV1 in the heart-lung transplant recipients, and BMI, HRpeak, VEpeak, FEV1, and number of days posttransplant in the lung transplant recipients. In addition to these variables, physical deconditioning and factors related to pharmacotherapy, infection, and rejection may also contribute to the decreased PWC observed in the transplant recipients.

Adolescent↗
PubMed2001

Resuscitation and evaluation of non-beating hearts obtained from asphyxiated dogs via autoperfusing heart-lung circuit.

BACKGROUND: The shortage of donor hearts has made use of non-beating hearts as cardiac grafts an attractive possibility for heart transplant candidates. The purpose of this study was to evaluate the utility of leukocyte-depleted hot shot cardioplegia for resuscitation of non-beating hearts obtained from asphyxiated dogs via an autoperfusing heart-lung circuit. METHODS: Mongrel dogs were divided into 3 groups according to the warm ischemia time and the method of reperfusion before starting the autoperfusing heart-lung circuit. Group A (n=4) had 60 minutes of warm ischemia and reperfusion without leukocyte-depleted hot shot, Group B (n=5) had 30 minutes of warm ischemia and reperfusion with leukocyte-depleted hot shot, and Group C (n=7) had 60 minutes of warm ischemia and reperfusion with leukocyte-depleted hot shot. We calculated stroke work via the heart-lung circuit to evaluate cardiac function of the resuscitated hearts. The criteria for "recovery" has been reported elsewhere. Myocardial water content of the resuscitated hearts was also measured and analyzed. No inotropic agents were used. RESULTS: The recovery rates in groups A, B and C were 0%, 80% and 57%, respectively, and the group B rate was significantly higher than the group A rate (p=0.04). Although myocardial water content did not differ between groups B and C, it was significantly lower in recovered hearts than in non-recovered hearts (p=0.04). Significant negative correlation was observed between the maximum stroke work value and myocardial water content in the resuscitated hearts (r=0.668, p=0.03). CONCLUSIONS: The autoperfusing heart-lung circuit is useful for evaluation and maintenance of cardiac function. Our experimental data shows that leukocyte-depleted hot shot plays a great role for resuscitation and recovery of non-beating hearts.

Animals↗
PubMed1997

Regulation of local angiotensin II formation in the human heart in the presence of interstitial fluid. Inhibition of chymase by protease inhibitors of interstitial fluid and of angiotensin-converting enzyme by Ang-(1-9) formed by heart carboxypeptidase A-like activity.

BACKGROUND: Data from in vitro studies suggest that both chymase and ACE contribute to the local generation of angiotensin (Ang) II in the heart. The enzyme kinetics under in vivo conditions are unclear. We thus studied the generation of Ang II by cardiac tissue in the presence of interstitial fluid (IF) that contains a variety of naturally occurring protease inhibitors. METHODS AND RESULTS: Ang I was incubated with heart homogenate in the presence of IF. IF obtained from human skin contained substantial amounts of protease inhibitors and ACE activity, the concentration of alpha 1-antitrypsin being 35% and the activity of ACE 24% of the corresponding serum values. When heart homogenate was incubated with Ang I, three enzymes were responsible for its metabolism: heart chymase and heart ACE converted Ang I to Ang II, and heart carboxypeptidase A (CPA)-like activity degraded Ang I to Ang-(1-9). Incubation of heart homogenate in the presence of IF led to practically full inhibition of heart chymase-mediated Ang II formation by the natural protease inhibitors present in IF. In contrast, heart CPA-like activity was not blocked, as reflected by the continued generation of Ang-(1-9). In addition, both heart ACE- and IF ACE-mediated Ang II formation were strongly inhibited. This inhibition was shown to be due to the Ang-(1-9) formed. CONCLUSIONS: The present experimental study defines two novel inhibitory mechanisms of Ang II formation in the human heart interstitium. Heart chymase-mediated Ang II formation is strongly inhibited by the natural protease inhibitors present in the IF. Similarly, both heart ACE- and IF ACE-mediated Ang II formation appear to be inhibited by the endogenous inhibitor Ang-(1-9) formed by heart CPA-like activity. These inhibitory mechanisms provide additional information about how the Ang II concentration in the heart interstitium may be controlled.

Angiotensin II↗
PubMed2003

Cholinergic stimulation with pyridostigmine reduces ventricular arrhythmia and enhances heart rate variability in heart failure.

BACKGROUND: Increased ventricular arrhythmia density and reduced heart rate variability are associated with risk of death in patients with heart failure. Cholinesterase inhibition with pyridostigmine bromide increases heart rate variability in normal subjects, but its effect on patients with heart failure is unknown. In this study, we tested the hypothesis that short-term administration of pyridostigmine bromide, a cholinesterase inhibitor, reduces ventricular arrhythmia density and increases heart rate variability in patients with congestive heart failure. METHODS: Patients with heart failure and in sinus rhythm participated in a double-blind, cross-over protocol, randomized for placebo and pyridostigmine (30 mg orally 3 times daily for 2 days). Twenty-four hour electrocardiographic recordings were performed for arrhythmia analysis and for the measurement of time domain indices of heart rate variability. Patients were separated into 2 groups, according to their ventricular arrhythmia density. The arrhythmia group (n = 11) included patients with >10 ventricular premature beats (VPBs) per hour (VPBs/h), and the heart rate variability group (n = 12) included patients with a number of VPBs in 24 hours not exceeding 1% of the total number of R-R intervals. RESULTS: For the arrhythmia group, pyridostigmine resulted in a 65% reduction of ventricular ectopic activity (placebo 266 +/- 56 VPBs/h vs pyridostigmine 173 +/- 49 VPBs/h, P =.03). For the heart rate variability group, pyridostigmine administration increased mean R-R interval (placebo 733 +/- 22 ms vs pyridostigmine 790 +/- 33 ms, P =.01), and in the time domain indices of heart rate variability root-mean-square of successive differences (placebo 21 +/- 2 ms vs pyridostigmine 27 +/- 3 ms, P =.01) and percentage of pairs of adjacent R-R intervals differing by >50 ms (placebo 3% +/- 1% vs pyridostigmine 6% +/- 2%, P =.03). CONCLUSION: In patients with heart failure, pyridostigmine reduced ventricular arrhythmia density and increased heart rate variability, most likely due to its cholinomimetic effect. Long-term trials with pyridostigmine in heart failure should be conducted.

Administration, Oral↗
PubMed1999

Native heart complications after heterotopic heart transplantation: insight into the potential risk of left ventricular assist device.

BACKGROUND: In heterotopic heart transplantation, the donor heart is connected parallel to the recipient's diseased heart. Recipients continue to have risks, such as arrhythmia, thromboembolism, valvular heart disease, and ischemic heart disease which can develop in the native heart. It may serve as a clinical model to study long-term pathophysiologic processes in the native heart of patients with a left ventricular assist device. METHOD: We analyzed the prevalence of long-term complications related to the native heart in the heterotopic heart transplant and attempted to gain insight into the potential risk to a native heart after receiving a left ventricular assist device. RESULTS: Between December 1984 and December 1994, 16 patients (13 men, 3 women, ranging in age from 37 to 60 years) underwent heterotopic heart transplant at the University of Pittsburgh. The 1- and 5-year survival rate after the transplant was 81% and 44%, respectively. Actuarial freedom from complications related to the native heart after 1 year and 4 years was ventricular arrhythmia: 85%, 75%; ischemic disease: 85%, 64%; valvular disease: 100%, 88%; and thromboembolism: 85%, 58%. Of these complications, thromboembolism was not considered in determining actuarial freedom from complications because thromboembolism should be regarded as a device-related complication rather than as a native-heart-related complication for left ventricular assist device recipients. Consequently, actuarial freedom from all complications excluding thromboembolism was 70% after 1 year and 50% after 4 years. In addition, the hazard function curve remains constant up to 80 months after the operation without significant differences among the yearly ratios. CONCLUSIONS: This analysis suggests that cautious observation of the native heart's long-term performance is necessary for the left ventricular assist device recipient.

Adult↗
PubMed1996

Impact of changes in respiratory frequency and posture on power spectral analysis of heart rate and systolic blood pressure variability in normal subjects and patients with heart failure.

1. Autonomic dysfunction is a major feature of congestive cardiac failure and may have an important role in determining progression and prognosis. The low-frequency/high-frequency ratio derived from power spectral analysis of heart rate variability has been proposed as a non-invasive method to assess sympatho-vagal balance. However, the effects of different respiratory rates or posture are rarely accounted for, but may be relevant in patients with heart failure in whom clinical improvement is accompanied by a fall in respiratory rate and an increased proportion of the day in the upright position. 2. We have assessed the effect of controlled respiration at different rates (10, 15, 20 breaths/min or 0.17, 0.25 and 0.33 Hz), while supine and standing, on power spectral analysis of heart rate and blood pressure variability in 11 patients with heart failure and 10 normal subjects. 3. Heart rate variance and low-frequency power (normalized units) were reduced in patients with heart failure (absent in six). During controlled breathing while supine, the power of the high-frequency component was significantly greater at 10 breaths/min than at 20 breaths/min in patients with heart failure, whether expressed in absolute units (P = 0.005) or percentage of total power (P = 0.03). 4. On standing, controlled breathing in patients with heart failure produced less change in high-frequency power (P = 0.054), but the low-frequency/high-frequency ratio at lower respiratory rates was reduced (P = 0.05). In normal subjects, as expected, respiratory rate had a highly significant effect on high-frequency power. Also, in normal subjects there was the expected increase in heart rate low-frequency power (P = 0.04) moving from supine to standing with an increase in the low-frequency/high-frequency ratio (P = 0.003), while in the patients with heart failure this was absent, reflecting blunted cardiovascular reflexes. 5. Systolic blood pressure low- and high-frequency components and their ratio were significantly affected by respiration (P < 0.03) and change in posture (P < 0.03) in both patients with heart failure and normal subjects, with a significant increase in the low-frequency/high-frequency ratio (P = 0.03) on standing in patients with heart failure, indicating that autonomic modulation of blood pressure is still operating in heart failure. 6. Thus, respiratory rate and changes in posture have a significant effect on measurements derived from spectral analysis of heart rate and blood pressure variability. Studies that use power spectral analysis as a measure of sympatho-vagal balance should control for these variables.

Adult↗
PubMed2001

Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure.

BACKGROUND: The independent prognostic value of elevated jugular venous pressure or a third heart sound in patients with heart failure is not well established. METHODS: We performed a retrospective analysis of the Studies of Left Ventricular Dysfunction treatment trial, in which 2569 patients with symptomatic heart failure or a history of it were randomly assigned to receive enalapril or placebo. The mean (+/-SD) follow-up was 32+/-15 months. The presence of elevated jugular venous pressure or a third heart sound was ascertained by physical examination on entry into the trial. The risks of hospitalization for heart failure and progression of heart failure as defined by death from pump failure and the composite end point of death or hospitalization for heart failure were compared in patients with these findings on physical examination and patients without these findings. RESULTS: Data on 2479 patients were complete and analyzed. In multivariate analyses that were adjusted for other markers of the severity of heart failure, elevated jugular venous pressure was associated with an increased risk of hospitalization for heart failure (relative risk, 1.32; 95 percent confidence interval, 1.08 to 1.62; P<0.01), death or hospitalization for heart failure (relative risk, 1.30; 95 percent confidence interval, 1.11 to 1.53; P<0.005), and death from pump failure (relative risk, 1.37; 95 percent confidence interval, 1.07 to 1.75; P<0.05). The presence of a third heart sound was associated with similarly increased risks of these outcomes. CONCLUSIONS: In patients with heart failure, elevated jugular venous pressure and a third heart sound are each independently associated with adverse outcomes, including progression of heart failure. Clinical assessment for these findings is currently feasible and clinically meaningful.

Aged↗
PubMed2003

Circulating levels of tumor necrosis factor correlate with indexes of depressed heart rate variability: a study in patients with mild-to-moderate heart failure.

OBJECTIVES: Patients with heart failure have increased circulating levels of tumor necrosis factor (TNF) and TNF receptors. It is not known whether TNF, which is known to blunt beta-adrenergic responsiveness in experimental models, contributes to the loss of heart rate variability in patients with heart failure. Therefore, we examined heart rate variability in relation to circulating levels of TNF, TNF receptors, and norepinephrine in patients with heart failure and in control subjects. METHODS: Heart rate variability was obtained from 24-h ambulatory ECG recordings in age-matched control subjects (n = 10) and patients with mild (n = 15) to moderate (n = 14) heart failure. Plasma levels of TNF and soluble type 1 and 2 TNF receptors were measured by enzyme-linked immunoassay; plasma norepinephrine levels were measured by high-performance liquid chromatography. RESULTS: There was a significant inverse linear correlation between increased circulating levels of TNF, TNF receptors, and norepinephrine for time-domain and frequency-domain indexes of heart rate variability among patients with heart failure and control subjects. Multiple stepwise linear regression analysis showed that TNF was a stronger independent predictor of frequency-domain indexes of heart rate variability than norepinephrine. CONCLUSIONS: TNF is an independent predictor of depressed heart rate variability in patients with heart failure. Insofar as TNF blunts beta-adrenergic signaling, this study suggests the possibility that overexpression of TNF and subsequent loss of beta-adrenergic responsiveness contributes to the decrease in heart rate variability observed in heart failure.

Case-Control Studies↗
PubMed1997

Six-minute walk test and heart rate variability: lack of association in advanced stages of heart failure.

BACKGROUND: The 6-minute walk and heart rate variability have been used to assess mortality risk in patients with heart failure, but their relationship to each other and their usefulness for predicting mortality at 1 year are unknown. OBJECTIVE: To assess the relationships between the 6-minute walk test, heart rate variability, and 1-year mortality. METHOD: A sample of 113 patients in advanced stages of heart failure (New York Heart Association Functional Class III-IV, left ventricular ejection < 0.25) were studied. All 6-minute walks took place in an enclosed, level, measured corridor and were supervised by the same nurse. Heart rate variability was measured by using (1) a standard-deviation method and (2) Poincaré plots. Data on RR intervals obtained by using 24-hour Holter monitoring were analyzed. Survival was determined at 1 year after the Holter recording. RESULTS: The results showed no significant associations between the results of the 6-minute walk and the two measures of heart rate variability. The results of the walk were related to 1-year mortality but not to the risk of sudden death. Both measures of heart rate variability had significant associations with 1-year mortality and with sudden death. However, only heart rate variability measured by using Poincaré plots was a predictor of total mortality and risk of sudden death, independent of left ventricular ejection fraction, serum levels of sodium, results of the 6-minute walk test, and the standard-deviation measure of heart rate variability. CONCLUSIONS: Results of the 6-minute walk have poor association with mortality and the two measures of heart rate variability in patients with advanced-stage heart failure and a low ejection fraction. Further studies are needed to determine the optimal clinical usefulness of the 6-minute walk and heart rate variability in patients with advanced-stage heart failure.

Death, Sudden↗
PubMed1999

Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease.

Three well-characterized mitogen-activated protein kinase (MAPK) subfamilies are expressed in rodent and rabbit hearts, and are activated by pathophysiological stimuli. We have determined and compared the expression and activation of these MAPKs in donor and failing human hearts. The amount and activation of MAPKs was assessed in samples from the left ventricles of 4 unused donor hearts and 12 explanted hearts from patients with heart failure secondary to ischaemic heart disease. Total MAPKs or dually phosphorylated (activated) MAPKs were detected by Western blotting and MAPK activities were measured by in gel kinase assays. As in rat heart, c-Jun N-terminal kinases (JNKs) were detected in human hearts as bands corresponding to 46 and 54 kDa; p38-MAPK(s) was detected as a band corresponding to approximately 40 kDa, and extracellularly regulated kinases, ERK1 and ERK2, were detected as 44- and 42-kDa bands respectively. The total amounts of 54 kDa JNK, p38-MAPK and ERK2 were similar in all samples, although 46-kDa JNK was reduced in the failing hearts. However, the mean activities of JNKs and p38-MAPK(s) were significantly higher in failing heart samples than in those from donor hearts (P<0.05). There was no significant difference in phosphorylated (activated) ERKs between the two groups. In conclusion, JNKs, p38-MAPK(s) and ERKs are expressed in the human heart and the activities of JNKs and p38-MAPK(s) were increased in heart failure secondary to ischaemic heart disease. These data indicate that JNKs and p38-MAPKs may be important in human cardiac pathology.

Animals↗
PubMed2002

In vitro motility analysis of thin filaments from failing and non-failing human heart: troponin from failing human hearts induces slower filament sliding and higher Ca(2+) sensitivity.

Contractility of the myocardium is altered in end-stage heart failure. We investigated whether this was related to functional changes in troponin. We isolated troponin from 1 g samples of end-stage failing, non-failing and foetal human heart and studied its regulation of actin-tropomyosin movement over immobilised HMM by in vitro motility assay. At pCa5.4 the sliding velocity of thin filaments reconstituted with non-failing heart troponin was 52+/-4% more than actin-tropomyosin, with failing heart troponin velocity increased by 35+/-2% and with foetal heart troponin velocity increased by 11+/-4%. Thin filaments containing troponin from failing hearts were more Ca(2+)-sensitive than non-failing heart troponin. EC(50) for the fraction of filaments motile and filament velocity decreased 1.76+/-0.20 and 1.89+/-0.62-fold respectively relative to non-failing heart troponin. With foetal heart troponin the EC(50) decreased 2.16+/-0.23 and 3.50+/-1.73-fold for fraction and velocity respectively. Western blots revealed no difference in troponin T or troponin I isoform expression in troponin from failing and non-failing adult hearts but foetal isoforms of troponin I and T were observed in troponin from foetal heart. The level of PKA phosphorylation of troponin from failing and non-failing heart was not significantly different, however, complete non-specific dephosphorylation of troponin abolished most of the difference between failing and non-failing heart troponin. These findings show functional alterations in troponin in failing hearts which could account for the reduced contractile function but there is no change in troponin isoform expression or PKA phosphorylation. Differential phosphorylation by other kinases may account for altered troponin function.

Actin Cytoskeleton↗
PubMed1997

The effects of simvastatin on the incidence of heart failure in patients with coronary heart disease.

BACKGROUND: Although treatment of myocardial overload effectively reduces death from progression of heart failure, it is not known whether the retardation of progressive coronary artery disease obtained with lipid lowering treatment will prevent the onset and consequences of heart failure in patients without previous symptoms of heart failure. METHODS AND RESULTS: In the Scandinavian Simvastatin Survival Study, 4444 patients with coronary heart disease without evidence of heart failure were randomized to placebo (n = 2223) or simvastatin 20-40 mg (n = 2221) and followed for more than 5 years. Among the patients who received placebo, 228 (10.3%) were diagnosed with heart failure during follow-up evaluation compared with 184 (8.3%) of patients who received simvastatin (P < .015). Mortality was 31.9% in the placebo group and 25.5% in the simvastatin group among patients who developed heart failure. These compare with 9.2 and 6.6%, respectively, among non-heart failure patients. There were 45 hospitalizations because of acute heart failure in the placebo group and 23 in the simvastatin group (NS). Patients who developed heart failure were more likely to have suffered a recurrent myocardial infarction and have a history of diabetes, peripheral artery disease, and hypertension than patients who did not develop congestive heart failure. CONCLUSION: Long-term prevention with simvastatin reduces the occurrence of heart failure in a cohort of patients with coronary heart disease without previous evidence of congestive heart failure.

Adult↗
PubMed2006

Association of parental heart failure with risk of heart failure in offspring.

BACKGROUND: The association between heart failure in parents and the prevalence of left ventricular systolic dysfunction and the risk of heart failure in their offspring has not been investigated in a community-based setting. METHODS: We examined the cross-sectional association of heart failure in parents with the prevalence of left ventricular systolic dysfunction, as well as left ventricular mass, internal dimensions, and wall thickness, in 1497 participants of the Framingham Offspring Study (mean age, 57 years; 819 women) who underwent routine echocardiography. We also investigated prospectively whether heart failure in parents increased the risk of heart failure in 2214 offspring (mean age, 44 years; 1150 women). RESULTS: As compared with the 1039 participants whose parents did not have heart failure, the 458 participants in the cross-sectional cohort who had at least one parent with heart failure were more likely to have increased left ventricular mass (17.0 percent vs. 26.9 percent), left ventricular internal dimensions (18.6 percent vs. 23.4 percent), and left ventricular systolic dysfunction (3.1 percent vs. 5.7 percent); the multivariable-adjusted odds ratios were 1.35 (95 percent confidence interval, 0.99 to 1.84), 1.29 (95 percent confidence interval, 0.96 to 1.72), and 2.37 (95 percent confidence interval, 1.22 to 4.61), respectively. In the longitudinal cohort, heart failure developed in 90 offspring during follow-up (mean length of follow-up, 20 years). The age- and sex-adjusted 10-year incidence rates of heart failure were 2.72 percent among offspring with a parent with heart failure, as compared with 1.62 percent among those without a parent with heart failure. This increase in risk persisted after multivariable adjustment (hazard ratio, 1.70; 95 percent confidence interval, 1.11 to 2.60). CONCLUSIONS: Heart failure in parents is associated with an increased prevalence of left ventricular systolic dysfunction cross-sectionally and an elevated risk of heart failure longitudinally. Our data emphasize the contribution of familial factors to the heart-failure burden in the community.

Adult Children↗
PubMed2006

Noninvasive coronary angiography with 64-section CT: effect of average heart rate and heart rate variability on image quality.

PURPOSE: To evaluate prospectively the effect of average heart rate and heart rate variability on image quality at 64-section computed tomographic (CT) coronary angiography. MATERIALS AND METHODS: The study protocol had local ethics committee approval; written informed consent was obtained. There were 125 patients (45 women, 80 men; mean age, 59.9 years +/- 12.9 [standard deviation]; 79 receiving beta-blockers) who underwent 64-section CT coronary angiography with retrospective electrocardiographic gating. Data sets were reconstructed in 5% steps from 20% to 80% of R-R interval. Heart rate variability was calculated as 1 standard deviation from mean rate during scanning. Two observers rated image quality of each coronary segment at least 1.5-mm diameter (1 = no motion artifacts, 5 = not evaluative). Repeated analysis of variance measurements were performed to evaluate quantitative parameters. Pearson correlation analysis was performed to compare image quality in each patient with average heart rate and heart rate variability. RESULTS: Average heart rate was 63.3 beats per minute +/- 13.1, with variability of 3.2 beats per minute +/- 2.1. Diagnostic image quality (score < or = 3) was attained in 1821 of 1836 segments at the best reconstruction interval. There was no correlation between mean heart rate and image quality for all segments of the right coronary and left anterior descending arteries, but there was a significant correlation for left circumflex artery (r = 0.33, P < .05). Heart rate variability was correlated with image quality overall (r = 0.75, P < .001) and for each coronary artery. Heart rate was less variable and image quality was better (P < .05) in patients receiving beta-blockers. Best image quality was obtained in diastole with heart rate less than 80 beats per minute and in systole with faster heart rate. CONCLUSION: Coronary angiography with 64-section CT provides diagnostic image quality within a wide range of heart rates. Reducing average heart rate and heart rate variability is beneficial for reducing artifacts.

Adult↗
PubMed2002

Alcohol consumption and risk for congestive heart failure in the Framingham Heart Study.

BACKGROUND: Although excessive alcohol consumption can promote cardiomyopathy, little is known about the association between alcohol consumption and risk for congestive heart failure in the community. OBJECTIVE: To determine the relation between alcohol consumption and risk for congestive heart failure in the community. DESIGN: Community-based, prospective observational study. SETTING: Framingham, Massachusetts. PARTICIPANTS: Participants in the Framingham Heart Study who were free of congestive heart failure and coronary heart disease. MEASUREMENTS: Self-reported alcohol consumption; sex-specific rates of congestive heart failure per 1000 person-years of follow-up by level of alcohol consumption. RESULTS: In men, 99 cases of congestive heart failure occurred during 26 035 person-years of follow-up. In women, 120 cases of congestive heart failure occurred during 35 563 person-years of follow-up. After adjustment for multiple confounders, risk for congestive heart failure was lower among men at all levels of alcohol consumption compared with men who consumed less than 1 drink/wk. The hazard ratio for congestive heart failure was lowest among men who consumed 8 to 14 drinks/wk (0.41 [95% CI, 0.21 to 0.81]) compared with those who consumed less than 1 drink/wk. In women, the age-adjusted hazard ratio for congestive heart failure was lowest among those who consumed 3 to 7 drinks/wk (0.49 [CI, 0.25 to 0.96]) compared with those who consumed less than 1 drink/wk. However, after adjustment for multiple predictors of congestive heart failure, this association was no longer statistically significant. CONCLUSIONS: In the community, alcohol consumption is not associated with increased risk for congestive heart failure, even among heavy drinkers (> or = 15 drinks/wk in men and > or = 8 drinks/wk in women). To the contrary, when consumed in moderation, alcohol appears to protect against congestive heart failure.

Adult↗
PubMed2003

Total recovery of heart grafts of non-heart-beating donors after 3 hours of hypothermic coronary oxygen persufflation preservation in an orthotopic pig transplantation model.

BACKGROUND: The coronary oxygen persufflation (COP) technique has been previously shown to allow prolonged heart preservation of 14 hr with optimal recovery in a pig model of orthotopic transplantation. This technique may be applicable to hearts grafted from non-heart-beating donors (NHBD). METHODS: Experiments were performed on pigs to test the effectiveness of oxygenated preservation, using COP for preservation of NHBD hearts. After 16 min of in situ normothermic ischemia, the hearts were flushed with histidine-tryptophan-ketoglutarate (HTK) solution or modified HTK solution (mBHTK) including 30 mmol/L 2,3-butanedione monoxime, 40 mg/L hyaluronidase,15 micromol/L adenosine, and 50 micromol/L calcium. Hearts were stored in the flush solutions for 3.3 hr or additionally persufflated with gaseous oxygen through the coronary arteries (COP) and transplanted orthotopically. RESULTS: Simple storage in HTK did not allow recovery of these hearts, whereas mBHTK storage resulted in improved function with 1.1 L/min cardiac output. The cardiac output reached 2.8 L/min (68% of normal values) with a left ventricular developed pressure of 101 mm Hg only after mBHTK+COP. Then the hearts were able to guarantee the circulation of the recipient for the test period after weaning from the heart-lung machine. CONCLUSIONS: Even in an NHBD with more than 15 min of in situ ischemia, the use of COP in combination with mBHTK solution for 3.3-hr storage of the heart allows excellent recovery of transplanted hearts and normal weaning from the heart-lung machine. This indicates that COP combined with mBHTK may be an optimal preservation technique for use with NHBD hearts.

Animals↗
PubMed2004

[Restoration of the heart activity in deep hypothermia with the aid of norepinephrine and no warming of the heart].

A possibility of restoration and stimulation of the rat isolated heart contractions in deep hypothermia by means of norepinephrine (6 microM) was studied. Following a complete arrest of the heart at a retrograde perfusion with the Krebs-Henseleit buffer ([K+] 5.9 mM), norepinephrine was found to restore the heart beats and to lower the heart arrest temperature from 8.2 +/- 0.5 degrees to 6.6 +/- 0.3 degrees. At the perfusion with the Krebs-Henseleit buffer, the heart rate dropped to below 10 min(-1) at 13.0 +/- 0.9 degrees. Reduction of [K+] to 2.95 mM intensified the heart rate. At a progressing cooling, the heart rate lower than 10 min(-1) occurred at 10.9 +/- 0.6 degrees. When adding norepinephrine (6 microM) to the perfusion fluid with [K+] 2.95 mM, the heart rate increased once again (on the average to 23.1 +/- 5.3 min(-1)) despite the fact that the heart temperature continued to be lowered. The heart rate lower than 10 min(-1) was reached at the progressing cooling to, on the average, 9.6 +/- 0.7 degrees. The findings show norepinephrine to exert a stimulating effect on the heart activity even at such low heart temperatures as 7-10 degrees with no preliminary warming of the heart.

Animals↗
PubMedDate not supplied

Evolution of hemodynamics after orthotopic heart and heart-lung transplantation: early restrictive patterns persisting in occult fashion.

Though successfully transplanted hearts respond in such a way that individuals remain remarkably asymptomatic, they do not function normally. Characterization of early hemodynamic patterns and their evolvement has not been done. The evolution of hemodynamic indices in 20 patients receiving orthotopic heart (n = 17) or combined heart-lung (n = 3) transplants is therefore documented. In 15 isolated heart recipients, right heart catheterization was performed at 24 to 48 hours, 1 to 2 weeks, 4 to 8 weeks, and greater than 3 months after surgery at the time of routine endomyocardial biopsy. Early, patients had elevated mean blood pressure (96 +/- 14 mm Hg, mean +/- standard deviation), mean right atrial pressure (15 +/- 6 mm Hg), right ventricular end-diastolic pressure (16 +/- 7 mm Hg), mean pulmonary artery pressure (30 +/- 7 mm Hg), and mean pulmonary capillary wedge pressure (19 +/- 6 mm Hg), but normal resting heart rate (96 +/- 14 beats/min) and cardiac output (5.6 +/- 1.6 L/min). Heart rate, blood pressure, and output did not change during follow-up, but right atrial pressure decreased dramatically (4 +/- 2 mm Hg at 3 months), as did right ventricular end-diastolic pressure (4 +/- 4 mm Hg), mean pulmonary artery pressure (21 +/- 8 mm Hg), and pulmonary capillary wedge pressure (11 +/- 4 mm Hg). Analysis of right heart filling dynamics revealed an abnormal inspiratory rise in mean right atrial pressure (15 +/- 6 and 27 +/- 7 mm Hg at 24 to 48 hours) that subsequently resolved. In eight patients whose resting follow-up right heart pressures normalized, rapid volume challenge uncovered occult restrictive right atrial pressure patterns that increased from 4 +/- 4 to 9 +/- 4 mm Hg after infusion of saline solution. Kussmaul's response was not apparent with prevolume infusion, but volume expansion caused appearance of this hemodynamic pattern. All patients had early evidence of tricuspid insufficiency, but in two patients, the Doppler regurgitant fraction was over 50%. These two individuals had hemodynamics similar to the other 15 patients initially, but in contrast, their right heart filling pressures did not change during follow-up. Other significant echocardiographic findings included enlarged atria and increased left ventricular mass in all patients. In two of three combined heart-lung transplant patients, similar hemodynamic patterns were evident. Rejection indices did not correlate with hemodynamic observations. Thus a characteristic evolvement of hemodynamics in heart and heart-lung transplants that mimic dynamics associated with restrictive myocardial disease is documented.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗