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PubMed1998

Characterization of metabolic responses to low-flow ischemia in intact pig hearts and isolated blood-perfused neonatal pig hearts.

UNLABELLED: There are different well established experimental models of low-flow ischemia. We examined metabolic variables during reduced coronary blood flow (CBF) in intact pig hearts and isolated neonatal pig hearts, producing similar degrees of postischemic dysfunction without infarction. The isolated hearts were perfused with red blood cell enriched buffer. In eight open-chest pigs mid-LAD flow was reduced to 70% for 60 min, followed by 120 min reperfusion. Myocardial segment lengths were recorded and regional coronary venous blood was sampled. In isolated piglet hearts CBF was reduced to 50% (n = 4), 25% (n = 4), and 10% (n = 17). Only when flow was reduced to 10% did hearts show signs of anaerobic metabolism. Mechanical function was recorded by a balloon in the left ventricle and coronary venous blood was sampled. Intact pig hearts showed release of protons, CO2, and lactate which peaked after 5-10 min of ischemia and thereafter stabilized at reduced levels. In contrast, in isolated neonatal hearts exposed to 10% CBF releases of protons, CO2, and lactate were stable during ischemia with no adaptational changes over time. In a separate group (n = 4), repetitive biopsies revealed no adaptational changes over time for adenosine triphosphate and creatine phosphate during 10% CBF. Contractile function was stably reduced during ischemia in both models. CONCLUSION: During reduced CBF "metabolic adaptation" occurs in intact pig hearts. In contrast, this feature is not present in isolated blood-perfused piglet hearts. The mechanisms responsible for these differences are uncertain. However, differences in metabolism between adult and neonatal hearts and different loading conditions during ischemia might contribute.

Adaptation, Physiological↗
PubMed1995

Risk factors of coronary heart disease and total mortality among elderly men with and without preexisting coronary heart disease. Finnish cohorts of the Seven Countries Study.

OBJECTIVES: We attempted to determine whether elevated levels of the classic coronary heart disease risk factors are associated with increased coronary risk and all-cause mortality among elderly men with and without coronary heart disease at baseline. BACKGROUND: The strength of any association between the classic coronary risk factors and survival among elderly men with and without coronary heart disease has not been established. METHODS: The classic coronary risk factor levels and risk of coronary events and total mortality during a 5-year follow-up interval were studied among men aged 65 to 84 years. Coronary events were fatal myocardial infarction (n = 71), any myocardial infarction (n = 96) and, among the men without disease, other nonfatal coronary heart disease events (n = 80). RESULTS: Among the 171 men with prevalent coronary heart disease, significant (p < 0.05) risk factors for fatal myocardial infarction (n = 42) in multivariate analyses were low high density lipoprotein cholesterol (odds ratio [OR] 0.2, 95% confidence interval [CI] 0.1 to 0.8 for 1-mmol/liter increase), high ratio of total to high density lipoprotein cholesterol (OR 1.4, 95% CI 1.1 to 1.7 for 1-U increase), and smoking more than nine cigarettes daily (OR 6.0, 95% CI 1.5 to 24.9 vs. values in men who had never smoked). Among the 476 men without prevalent coronary heart disease, only high serum total cholesterol was a risk factor for fatal myocardial infarction (n = 29) (OR 1.4, 95% CI 1.0 to 2.0 for 1-mmol/liter increase). Among men with prevalent coronary heart disease, the only significant (p < 0.05) risk factor for total mortality was smoking more than nine cigarettes daily (OR 3.9, 95% CI 1.1 to 13.4 vs. values among men who had never smoked). Among men without prevalent coronary heart disease, only the use of antihypertensive medication (OR 2.0, 95% CI 1.2 to 3.3 between men with and without such medication) was a risk factor for total mortality. CONCLUSIONS: The classic risk factors for coronary heart disease appear to be of importance even in old age, especially among men with prevalent coronary heart disease.

Age Factors↗
PubMed2001

Community-wide coronary heart disease mortality in Mexican Americans equals or exceeds that in non-Hispanic whites: the Corpus Christi Heart Project.

PURPOSE: Previous comparisons of coronary heart disease mortality between Mexican Americans and non-Hispanic whites have given paradoxic results: despite their adverse cardiovascular risk profiles, especially a greater prevalence of diabetes, Mexican Americans are reported to have lower rates of mortality from coronary heart disease. SUBJECTS AND METHODS: We performed a community-based surveillance among all residents of Nueces County, Texas, aged 25 to 74 years, from 1990 to 1994. All death certificates were obtained and coded, and deaths potentially related to coronary heart disease were selected and validated by standardized methods blinded to ethnicity. Validated in-hospital and out-of-hospital coronary heart disease mortality was compared between 785 Mexican Americans and 862 non-Hispanic white women and men. RESULTS: Validated coronary heart disease mortality in Mexican Americans exceeded that for non-Hispanic whites in the same community. Among women, definite coronary heart disease mortality was 40% greater among Mexican Americans (rate ratio [RR] 1.43, 95% confidence interval [CI]: 1.12 to 1.82), as was all coronary heart disease mortality (RR, 1.32, 95% CI: 1.08 to 1.63). Among men, Mexican Americans had greater rates of all (RR, 1.11; 95% CI: 0.96 to 1.28) and definite coronary heart disease mortality (RR, 1.16; 95% CI: 0.91 to 1.47), but the associations were not statistically significant. CONCLUSIONS: When community-wide mortality rates from coronary heart disease are properly validated, Mexican Americans have rates equal to or higher than those of non-Hispanic whites. Community-based surveillance with validation of coronary heart disease as the cause of death is necessary to avoid the errors that occur with the use of death certificates alone.

Adult↗
PubMed2001

Ischaemic heart disease and Cag A strains of Helicobacter pylori in the Caerphilly heart disease study.

OBJECTIVE: To look for the presence of the more virulent strains of Helicobacter pylori (H pylori) in men who developed ischaemic heart disease over a 10 year period and in controls. DESIGN: The Caerphilly prospective heart disease study recruited 2512 men aged 45-59 years during 1979-83. Western blot analysis or enzyme linked immunosorbent assay (ELISA) was performed on serum taken from those who subsequently died of ischaemic heart disease, or developed non-fatal myocardial infarction, to determine H pylori and Cag A status. Similar information was available on age matched controls. RESULTS: During the first decade of the study, 312 men died of ischaemic heart disease or developed non-fatal myocardial infarction. Serum was available from 172 of these (55%). There was no evidence of an association between Cag A seropositivity and incident ischaemic heart disease or ischaemic heart disease mortality, either before or after adjustment for potential confounders (adjusted odds ratios 1.18 (95% confidence interval (CI) 0.76 to 1.85) and 1.13 (95% CI 0.61 to 2.07), respectively). Further, the odds ratios for ischaemic heart disease incidence and ischaemic heart disease mortality by H pylori seropositivity did not appear to depend on the presence or absence of Cag A strains (p = 0.76 and 0.77, respectively). CONCLUSIONS: In this cohort of middle aged men, followed over a 10 year period, there is little evidence of an association between Cag A seropositivity and either incident ischaemic heart disease or ischaemic heart disease mortality.

Antigens, Bacterial↗
PubMed2005

Increasing heart size and age attenuate anesthetic preconditioning in guinea pig isolated hearts.

Anesthetic preconditioning (APC) reduces myocardial ischemia/reperfusion injury. Recent investigations have reported that older hearts are not susceptible to APC. We investigated if increasing heart size with age determines the susceptibility to APC in young guinea pigs. Langendorff-prepared guinea pig hearts of different weights (1.1-2.2 g) and ages (2-7 wks) were exposed to 1.3 mM sevoflurane for 15 min followed by 30 min washout (APC; n = 20) before 30 min global ischemia and 120 min reperfusion. Control hearts (n = 20) were not subject to APC. Left ventricular pressure was measured isovolumetrically and infarct size was determined by triphenyltetrazolium staining. Functional data were not different between groups at the beginning of the experiments nor did they correlate with heart weight or age. At 120 min reperfusion, left ventricular pressure, coronary flow, and tissue viability showed significant negative correlations with increasing heart weight and age in APC but not in control hearts; i.e., APC improved function and attenuated infarct size better in smaller/younger hearts than in larger/older hearts. Thus, increasing age and heart size attenuate the susceptibility for APC even in younger guinea pigs. This may have important implications for further basic science research and the possible clinical applicability of APC in humans.

Aging↗
PubMed2003

Endothelin-1 concentrations in pericardial fluid are more elevated in patients with ischemic heart disease than in patients with nonischemic heart disease.

There is epidemiologic evidence that the prognosis of patients with nonischemic heart failure is better than that for patients with ischemic heart failure. In addition, studies have revealed that patients with ischemic heart failure show a poorer response to medical therapy. However, the pathophysiologic difference between ischemic and nonischemic heart disease is unclear. To clarify this point, we measured atrial natriuretic peptide, brain natriuretic peptide, angiotensin II, endothelin (ET)-1. interleukin-1beta interleukin-6. tumor necrosis factor (TNF)-alpha soluble TNF receptor I, and soluble TNF receptor II concentrations in plasma and pericardial fluid in patients with ischemic or nonischemic heart disease undergoing cardiac surgery. The pericardial ET-1 concentration in patients with ischemic heart disease was statistically greater than that in patients with nonischemic heart disease (about 1.5-fold), although no difference was found in the plasma ET-1 concentration. These findings suggest that the production and secretion of ET-1 from the myocardium in patients with ischemic heart disease are augmented to a greater extent than in patients with nonischemic heart disease. This result may lead to a greater understanding of the pathophysiology of ischemic heart disease.

Angiotensin II↗
PubMed2002

Heart weight and heart weight/body weight coefficient in malnourished adults.

OBJECTIVE: To compare the heart weight and the heart weight/body weight coefficient of adults with and without chronic malnutrition. METHODS: In an initial case series of 210 autopsies performed in adults, we recorded body and heart weights and calculated the heart weight/body weight coefficients (HW/BW x 100). The exclusion criteria were as follows: positive serology for Chagas' disease, edema, obesity, heart diseases, hepatopathies, nephropathies, and systemic arterial hypertension. Malnutrition was characterized as a body mass index <18.5kg/m2. Differences with p<0.05 were considered significant. RESULTS: Individuals in the malnourished (n=15) and control (n=21) groups were statistically different, respectively, in regard to body mass index (15.9+/-1.7 versus 21.3+/-2.5kg/m2), heart weight (267.3+/-59.8 versus 329.1+/-50.4g), and the HW/BW coefficient (0.64+/-0.12 versus 0.57+/-0.09%). A positive and significant correlation was observed between heart weight and body mass index (r=0.52), and between heart weight and body weight (r=0.65). CONCLUSION: Malnourished individuals have lighter hearts and a greater HW/BW coefficient than non-malnourished individuals do. These findings indicate a possible preservation of the myocardium in relation to the intensity of weight loss associated with the probable relative increase in cardiac connective tissue and heart blood vessels.

Adult↗
PubMed2001

Angiotensinogen mutations and risk for ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease. Six case-control studies from the Copenhagen City Heart Study.

BACKGROUND: The M235T and T174M angiotensinogen mutations have been linked to increased risk for ischemic heart and cerebrovascular disease. OBJECTIVE: To determine whether angiotensinogen mutations are associated with ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease. DESIGN: Six case-control studies from the Copenhagen City Heart Study. SETTING: Copenhagen, Denmark. PARTICIPANTS: Participants in the Copenhagen City Heart Study and patients from the same hospital with ischemic heart disease (n = 866 and n = 943, respectively), myocardial infarction (n = 519 and n = 493, respectively), or ischemic cerebrovascular disease (n = 489 and n = 434, respectively) and 7975 controls without these conditions. MEASUREMENTS: Genotypes for the M235T and T174M angiotensinogen mutations were compared between controls and Copenhagen City Heart Study participants with ischemic heart disease, myocardial infarction, and cerebrovascular disease (studies 1a, 1b, and 1c) and patients from Copenhagen University Hospital with the same conditions (studies 2a, 2b, and 2c). RESULTS: Relative allele frequencies of 235T and 174M in the general population were 0.41 and 0.12, respectively. Genotype was not associated with increased risk for ischemic heart or ischemic cerebrovascular disease in studies of either mutation alone or combined in women or men. Among compound heterozygotes (235MT /174TM ), women in case-control study 2a had decreased risk for ischemic heart disease in age-adjusted analysis; however, this decreased risk was not seen in multifactorial-adjusted or matched analyses, in men, or in case-control study 1a. Among double homozygotes (235TT /174MM ), women in case-control study 2b had increased risk for myocardial infarction in matched analysis; however, this increased risk was not seen in age- or multifactorial-adjusted analyses, in men, or in case-control study 1b. Among single homozygotes (235TT /174TT ), men in case-control study 2b had increased risk for myocardial infarction in multifactorial-adjusted and matched analyses. This risk was not present in age-adjusted analysis, in women, or in case-control study 1b. In addition, male single homozygotes had decreased risk for ischemic cerebrovascular disease in case-control study 2c in age- and multifactorial-adjusted analyses, but this finding was not seen in matched analysis, in women, or in case-control study 1c. CONCLUSIONS: In six large case-control studies, the M235T and T174M angiotensinogen mutations were not consistently associated with increased (or decreased) risk for ischemic heart disease, myocardial infarction, or ischemic cerebrovascular disease. Statistically significant associations may represent chance findings rather than real phenomena.

Aged↗
PubMedDate not supplied

External pacing does not potentiate allopurinol protection of the heart from liver ischemia-reperfusion -- a study in an isolated perfused liver-heart rat model.

BACKGROUND: We recently demonstrated that isolated paced hearts perfused with modified Krebs-Henseleit solution containing high dose allopurinol (1 mM) were protected from liver ischemia-reperfusion (IR)-induced reperfusion injury. The objective was to study the effects of low dose allopurinol together with external pacing in attenuating myocardial reperfusion dysfunction following liver IR in the same double organ model. MATERIAL AND METHODS: Isolated rat livers were perfused with modified Krebs-Henseleit solution (groups 1 and 2, n=8/all groups) or underwent global ischemia (groups 3-6) for 120 minutes. Following a 15-minute conjoint reperfusion of earlier separately isolated liver+heart, the hearts were recirculated alone for additional 45 minutes. The organs of three-group donating animals (groups 2, 4, and 6) were treated with allopurinol 18 hours and 1 hour before the experiment (50 mg x kg(-1) intraperitoneally) and it was also added during perfusion (0.1 mM in Krebs). The hearts in groups 5 and 6 were paced (300 x min(-1)). RESULTS: The hearts perfused with IR Krebs (group 3) experienced decreased myocardial left ventricular-developed pressure (LVP), heart rate (in the unpaced hearts) and later coronary flow (by 68%, 21% and 32%, respectively); LVP and coronary flow also decreased correspondingly in the IR-paced hearts (group 4). Xanthine oxidase (XO) was high in groups 3 and 4 compared to group 1. IR allopurinol-treated hearts, both unpaced and paced (groups 5 and 6) had normal, similar myocardial performance, while their circulating XO was as low as in group 2 (allopurinol-treated controls). CONCLUSIONS: External pacing in the double organ, isolated-perfused liver-heart did not ameliorate XO-mediated dysfunction compared to low dose allopurinol. The unexpected delayed coronary insufficiency in myocardial reperfusion injury is discussed.

Allopurinol↗
PubMed1992

Diet and coronary heart disease. The National Heart Foundation of Australia.

Over the last four decades there has been extensive research into the links between diet and coronary heart disease. The most recent literature is reviewed in this position statement. The clinical and public health aspects of the National Heart Foundation's nutrition policy are based on this review. The key points are as follows: 1. Saturated fatty acids A high intake of saturated fatty acids is strongly associated with elevated serum cholesterol and LDL-cholesterol levels and increased risk of coronary heart disease. 2. The n-6 polyunsaturated fatty acids The n-6 polyunsaturated fatty acids (principally linoleic acid) lower serum cholesterol levels when substituted for saturated fats and probably have an independent cholesterol-lowering effect. 3. The n-3 polyunsaturated fatty acids (fish oils) The n-3 polyunsaturated fatty acids reduce serum triglyceride levels, decrease the tendency to thrombosis and may further reduce coronary risk through other mechanisms. 4. Monounsaturated fatty acids Monounsaturated fatty acids reduce serum cholesterol levels when substituted for saturated fatty acids. It is not clear whether this is an independent effect or simply the result of displacement of saturates. 5. Trans fatty acids Trans fatty acids may increase serum cholesterol levels and can be reckoned to be equivalent to saturated fatty acids. 6. Total fat Total fat intake, independent of fatty acid type, is not strongly associated with coronary heart disease but may contribute to obesity. Associations between total fat intake and coronary heart disease are primarily mediated through the saturated fatty acid component. 7. Dietary cholesterol Dietary cholesterol increases serum cholesterol levels in some people and may increase risk of coronary heart disease. 8. Alcohol A high intake of alcohol increases blood pressure and serum triglyceride levels and increases mortality from cardiovascular disease. Light alcohol consumption reduces the risk of coronary heart disease. 9. Sugar The consumption of sugar is not associated with coronary heart disease. 10. Sodium and potassium High salt intake is related to hypertension especially in the subset of "salt-sensitive" people. Potassium intake may be inversely related to hypertension. 11. Overweight and obesity Abdominal obesity increases the risk of coronary heart disease probably by adversely influencing conventional risk factors. 12. Vegetarianism A high intake of plant foods reduces the risk of coronary heart disease through several mechanisms, including lowering serum cholesterol and blood pressure levels.

Alcohol Drinking↗
PubMed1984

Fatty acid binding protein from rat heart. The fatty acid binding proteins from rat heart and liver are different proteins.

The binding of [3H]oleic acid and [3H]palmitic acid to the low molecular weight fatty acid binding proteins present in the cytosols of rat liver and heart was studied. Both fatty acids were bound by Z protein of liver, whereas only oleic acid was bound by the fraction of heart that contains the fatty acid binding protein. However, after delipidation of heart cytosolic proteins with butanol, the binding of palmitic acid to the fatty acid binding protein was detected. In contrast to a published report (Gloster, J., and Harris, P. (1977) Biochem. Biophys. Res. Commun. 74, 506-513), oleic acid was not bound by rat heart or bovine heart myoglobin. Both rat heart fatty acid binding protein and rat liver Z protein were purified to homogeneity or near homogeneity. On polyacrylamide gel electrophoresis under nondenaturing conditions, liver Z protein gave rise to three bands, none of which was identical with the single band due to heart fatty acid binding protein. Rabbit antibodies to rat liver Z protein were used to demonstrate that the purified fatty acid binding protein from rat liver (Z protein) and rat heart are immunologically unrelated and that no Z protein is present in rat heart cytosol. Taken together, these observations lead to the conclusion that the low molecular weight fatty acid binding proteins from rat liver and heart are different proteins.

Animals↗
PubMed1993

Impact of heart rate and PR interval on Doppler indexes of left ventricular diastolic filling in an elderly cohort (the Framingham Heart Study).

The relations of heart rate and PR interval to Doppler-derived diastolic indexes were examined in 260 men (mean age 75 years) and 462 women (mean age 76 years) from the Framingham Heart Study. Subjects receiving any antihypertensive or cardiac medications were excluded from eligibility; those with mitral stenosis or prosthesis, pacemaker, atrial fibrillation, arrhythmia, left bundle branch block, congestive heart failure, previous myocardial infarction, and technically inadequate Doppler study were also excluded. Peak velocity of early (E) and late (A) diastolic left ventricular (LV) filling, ratio of peak velocities E/A, ratio of time velocity integrals E/A, and atrial filling fraction were studied by multivariable analyses adjusting for age, sex, blood pressure, heart rate and PR interval. Heart rate was a major determinant of all 5 Doppler indexes of diastolic filling; heart rate was inversely associated with peak velocity E, E/A, and time velocity integral E/A, and was directly associated with peak velocity A and atrial filling fraction. PR interval was inversely associated with time velocity integral E/A (p < 0.01) and directly associated with atrial filling fraction. The results were largely unaltered after further adjustment for LV wall thickness, LV end-diastolic diameter and left atrial diameter (in addition to age, sex and blood pressure). Heart rate and PR interval are independent contributors to Doppler-assessed LV diastolic filling in the elderly. The atrial contribution to LV filling depends on its timing in the cardiac cycle and on heart rate. Failure to account for heart rate and PR interval may lead to inappropriate assessment of Doppler diastolic filling.

Aged↗
PubMed1991

Beat-to-beat variation of heart rate in diabetic patients with autonomic neuropathy and in completely cardiac denervated patients following orthotopic heart transplantation.

Dysfunction of the vagal nerve, an early symptom in the development of autonomic neuropathy, can be assessed reliably by the beat-to-beat variation in heart rate. Patients after a cardiac transplantation are a unique model to investigate the beat-to-beat variation of a completely denervated heart. Heart rate and the beat-to-beat variation during normal and deep respiration were investigated in diabetic subjects with an autonomic neuropathy (n = 10), age and sex matched healthy controls (n = 10) and cardiac transplanted patients (n = 10). Further studies during pharmacological blockade of the parasympathetic nervous system with atropine were performed. In the denervated heart the coefficient of variation of the beat-to-beat interval was 0.38 +/- 0.02% during normal respiration, compared to 1.32 +/- 0.13% (P less than 0.0001) and 2.56 +/- 0.13% (P less than 0.0001) in the diabetic and control subjects, respectively. Administration of atropine (2 mg intravenously) decreased the coefficient of variation of the RR-interval to 0.73 +/- 0.09% in the diabetic patients (P less than 0.0005) and to 0.67 +/- 0.07% in the controls (P less than 0.0001), whereas the coefficient of variation remained unaffected in the cardiac denervated patients (0.39 +/- 0.02%). In the three groups an almost parallel increase of the RR-variation was observed during deep respiration at a rate of 6 breaths/min (from 0.38 +/- 0.02% to 1.99 +/- 0.38% in cardiac transplanted patients, P less than 0.0025; from 1.32 +/- 0.13% to 3.10 +/- 0.43% in diabetic patients, P less than 0.0025; from 2.56 +/- 0.13% to 5.42 +/- 0.94% in healthy controls, P less than 0.005). We conclude that a beat-to-beat variation of heart rate is present in the completely denervated heart. This RR-variation can not be influenced by a pharmacological blockade of the parasympathetic nervous system with atropine. The beat-to-beat variation increases during deep respiration not only in healthy controls but also in diabetic patients with autonomic neuropathy (partially denervated hearts) and cardiac transplanted patients (completely denervated hearts). This indicates an intracardiac mechanism in the modulation of heart rate.

Atropine↗
PubMed1993

Hemodynamic correlates of the third heart sound during the evolution of chronic heart failure.

OBJECTIVES: The purpose of this study was to examine the temporal relation between the development of a third heart sound during the course of evolving heart failure and associated hemodynamic abnormalities. BACKGROUND: Although various theories have been proposed to explain the origin of the third heart sound, the exact origin of this sound remains unknown. METHODS: Studies were performed in seven dogs in which heart failure was produced by multiple sequential intracoronary micro-embolizations. Hemodynamic studies including ventriculography, pulsed wave Doppler echocardiography and intracardiac phonocardiography were performed at baseline, at the time at third heart sound was first heard and at 6 and 24 weeks after onset of the third heart sound. RESULTS: All dogs developed a third heart sound at 9 +/- 2 weeks after the initial embolization. The onset of the sound was accompanied by an increase in left ventricular chamber stiffness relative to the baseline value (0.25 +/- 0.03 vs. 0.14 +/- 0.01 mm Hg/ml) (p < 0.05) and mean deceleration of early mitral inflow velocity (1,040 +/- 90 vs. 590 +/- 40 cm/s per s) (p < 0.05). CONCLUSIONS: These data indicate that the onset of a third heart sound during the course of evolving heart failure occurs coincident with the development of increased left ventricular chamber stiffness and the manifestation of rapid deceleration of early mitral inflow velocity. These findings are consistent with a myocardial vibratory origin of this sound.

Animals↗
PubMed1989

Heart- and heart-lung transplantation in children.

Since January 1987, 16 prepubertal children have undergone heart (13) or heart-lung (3) transplantation. Immunosuppression included cyclosporine and azathioprine and excluded steroids except in case of rejection. The indications for heart transplantation were hypoplastic left heart syndrome (4 infants, mean age = 2 months), congenital heart disease (4 patients, mean age = 5.7 years) and cardiomyopathy (5 patients, mean age = 2.8 years). There were 4 early deaths (acute graft failure in 2, pulmonary hypertension in 1, infection in 1) and 1 late death (heart failure at 3 months). The 8 survivors had a mean follow-up of 12 months (range 1-19 months). Late complications were minimal. There were 4 episodes of rejection in 2 patients. There was no infection, normal somatic growth and no systemic hypertension. Renal function remained within normal limits although mild-to-moderate tubulointerstitial lesions were found in 4 renal biopsies. Three children (9-11 years old) underwent heart-lung transplantation. The early postoperative course was difficult with 6 episodes of rejection and 5 infections. One patient died at 3 months from infectious complications. One child has a complete rehabilitation 8 months posttransplantation. The last patient is clinically well at 7 months but has a residual tracheal stenosis. The long-term fate of these children, and particularly the long-term effects of cyclosporine therapy are unknown. Heart and heart-lung transplantation remain under investigation but may be reasonable approaches for infants and children with end-stage cardiac and/or pulmonary disease.

Acute Kidney Injury↗
PubMed2005

Sympathetic neuronal regulation of the heart in aging and heart failure.

The documentation of preferential activation of the cardiac sympathetic outflow in patients with heart failure swept aside an entrenched notion that there was a functional sympathetic denervation of the failing heart and provided a theoretical basis for the clinical evaluation of beta-adrenergic blocker therapy in this condition. The demonstration that heightened sympathetic nervous system activity is central to the pathogenesis and progression of congestive heart failure (CHF) has now led to the rational use of beta-adrenoceptor blockade in CHF. More recently, it has also emerged that the aging heart exhibits some of the characteristic changes in autonomic control which are seen in CHF. Accordingly, alterations in cardiac sympathetic nerve function are now thought to contribute also to the pathophysiology of the aging heart. Furthermore, there is evidence that in humans, sympathoexcitatory rostral projections of brainstem noradrenergic neurons to the forebrain are important in the sympathetic nervous activation of both heart failure and aging. Given these similarities, in this review we compare and contrast the neurobiology of the sympathetic nervous system in the failing heart and the healthy, aging heart, and consider whether the sympathetic activation accompanying aging may, perhaps, underlie and contribute to the neural pathophysiology of heart failure. Our conclusion is, on balance, that this proposition is not supported by the available evidence.

Adrenal Glands↗
PubMed2006

Cardiac resynchronization therapy delays heart transplantation in patients with end-stage heart failure and mechanical dyssynchrony.

BACKGROUND: Cardiac dyssynchrony is frequent in advanced heart failure, and cardiac resynchronization therapy (CRT) may offer an alternative to heart transplantation. We aimed to investigate the impact of CRT on freedom from Tx and death in transplant candidates with end-stage heart failure. METHODS: Over a period of 2 years, 46 consecutive patients with refractory congestive heart failure due to dilated cardiomyopathy were referred for heart transplant evaluation. Patients with cardiac dyssynchrony > 107 milliseconds according to tissue Doppler imaging (TDI) or QRS duration > 150 milliseconds were treated with CRT (CRT group, n = 24), whereas patients without dyssynchrony were not treated (non-CRT group, n = 22). RESULTS: At baseline, both groups showed similar hemodynamic and functional parameters, including ejection fraction (19 +/- 10% vs 21 +/- 12%, not statistically significant [NS]) and Vo2max (11.9 +/- 2.0 vs 12.0 +/- 1.8 ml/kg/min, NS). After a follow-up of 488 +/- 346 days, cumulative survival with freedom from transplantation and death was higher in CRT vs non-CRT patients (92% vs 39%; p < 0.001). CRT patients showed a decrease in New York Heart Association (NYHA) class from 3.2 +/- 1.1 to 2.2 +/- 0.9 (p = 0.003) and an increase in Vo2max from 11.9 +/- 2.0 to 13.1 +/- 1.8 ml/kg/min (p = 0.02), and 71% (17 of 24) of these patients were successfully removed from the waiting list. CONCLUSIONS: In heart transplant candidates with significant dyssynchrony, CRT delays heart transplantation and improves NYHA class and exercise capacity. For these patients, CRT should be considered before heart transplantation.

Aged↗
PubMed2006

Association of heart rate recovery and maximum oxygen consumption in patients with chronic congestive heart failure.

BACKGROUND: Peak oxygen consumption (peak VO2) is one of the strongest predictors of mortality in patients with congestive heart failure (CHF). In contrast to measurements of peak VO2, which requires analysis of expired gases, heart rate recovery, defined as maximum heart rate minus heart rate at 1 minute after exercise, is easily obtained. The current study was undertaken to determine the association between peak VO2 and heart rate recovery in patients with CHF. METHODS: Retrospective data on VO2 and heart rate recovery were analyzed in 296 patients with CHF secondary to left ventricular systolic dysfunction (left ventricular ejection fraction [LVEF] <50%) who had undergone cardiopulmonary exercise testing (CPET). Patients exercised on a treadmill using a graded work rate protocol with the work increasing to a symptom-limited maximum. Peak oxygen consumption was defined as the highest value of oxygen uptake attained in the final 20 seconds of exercise when the respiratory exchange ratio was >1.0. RESULTS: Heart rate recovery and peak VO2 correlated moderately (r = 0.47, p < 0.001). The degree of correlation was similar in patients receiving beta-blockers (r = 0.47, p < 0.001) and those not receiving beta-blockers (r = 0.49, p < 0.001). CONCLUSIONS: Although heart rate recovery and peak VO2 correlated moderately, from a clinical standpoint, this finding is probably not strong enough to use heart rate recovery in lieu of peak VO2. This modest correlation of two independent predictors of outcome may suggest their usefulness when combined in a multivariate score.

Chronic Disease↗