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At least 505 records · Page 28Linked to original sources
PubMed2005

Management of heart failure in primary care after implementation of the National Service Framework for Coronary Heart Disease: a cross-sectional study.

OBJECTIVES: To compare the management of heart failure with the standards set out in the National Service Framework for Coronary Heart Disease. STUDY DESIGN: A cross-sectional study in 26 general practices, with a combined list size of 256,188, that are members of the Kent, Surrey and Sussex Primary Care Research Network. METHODS: Information was extracted on the management of 2129 patients with heart failure, of whom 2097 were aged 45 years and over. RESULTS: The prevalence of heart failure was 8.3 per 1000. Prevalence rates increased with age, from 0.2 per 1000 in people aged under 35 years of age to 125 per 1000 in those aged 85 years and over. Coronary heart disease (present in 47%) was the most common comorbid condition in men with heart failure, whereas hypertension (present in 46%) was the most common condition in women. Recording of cardiovascular risk factors was generally higher in younger patients than in older patients, and in men than in women. Blood pressure (92% of men and 90% of women) and smoking status (84% of men and 77% of women) were generally the best-recorded cardiovascular risk factors. Blood electrolytes were recorded in about 83% of men and 75% of women. Only 17% of men and 11% of women with heart failure had a record of undergoing an echocardiogram. Use of angiotensin-converting enzyme (ACE) inhibitors or antagonists was 76% in men with heart failure and 68% in women; lowest rates were seen in older patients. Uptake of influenza immunization was generally high, at 85% in men and 84% in women. CONCLUSIONS: The use of ACE inhibitors in patients with heart failure was higher than in some previous studies. However, many patients have no documentation in their computerized medical records of having undergone key investigations, such as echocardiography.

Adult↗
PubMed2006

Troponin phosphorylation and regulatory function in human heart muscle: dephosphorylation of Ser23/24 on troponin I could account for the contractile defect in end-stage heart failure.

We made quantitative measurements of phosphorylation in troponin isolated from 6 non-failing donor hearts and 6 explanted hearts with end-stage heart failure in SDS-PAGE gels using Pro-Q Diamond phosphoprotein stain. The troponin T phosphorylation level was the same in troponin from failing and non-failing heart (3.1 mol Pi/mol). However, troponin I phosphorylation was significantly lower in failing (0.37+/-0.18 mol Pi/mol) compared with non-failing heart troponin (2.25+/-0.36 mol Pi/mol). Levels of troponin I PKA-dependent phosphorylation, measured with a phosphoserine 23/24-specific antibody, were also significantly lower in failing heart troponin (0.19+/-0.06 mol Pi/mol) compared to non-failing troponin (1.14+/-0.09 mol Pi/mol). We calculate that there is phosphorylation in addition to serine 23/24 of 1.11+/-0.34 mol Pi/mol in non-failing reduced to 0.18+/-0.17 mol Pi/mol in failing heart troponin, attributed to phosphorylation on the PKC sites. To test for the functional role of troponin I phosphorylation, the native troponin I from either non-failing or failing heart troponin was exchanged for a recombinant (unphosphorylated) human cardiac troponin I. Thin filament Ca(2+)-regulatory function was studied with the quantitative in vitro motility assay: thin filaments containing the replaced troponin I resulted in a failing phenotype of a 17-26% reduced sliding speed and an increased Ca(2+)-sensitivity relative to non-failing troponin (EC(50) TnI-exchanged/non-failing=0.57, p<0.001). When exchanged with troponin I phosphorylated with PKA motility parameters reverted to a pattern indistinguishable from non-failing troponin (p=0.35-0.75). We suggest that changes in troponin function can account for the contractile abnormality in failing heart muscle and that the functional changes in troponin are due to reduced phosphorylation of troponin I at the PKA sites.

Adult↗
PubMed2002

Effects of autologous platelet concentrate reinfusion after open heart surgery in patients with congenital heart disease.

BACKGROUND: Plasma pheresis and reinfusion of platelet-rich plasma has not been shown to reduce blood loss in cardiac patients. Recently, freshly prepared autologous platelet concentrates (PC) can be made from patient's blood and has a higher concentration than conventional platelet rich plasma. In this study, the effects of autologous PC reinfusion were examined after open heart surgery in patients with congenital heart disease. METHODS: Eight patients with noncyanotic congenital heart disease, who underwent open heart surgery and reinfusion of autologous PC, were classified as the PC group. Eight other patients with noncyanotic congenital heart disease, who underwent only open heart surgery, were defined as the control group. Ages ranged from 2 to 24 years and were not significantly different between the two groups (9.3 +/- 5.1 years in the PC group and 12.6 +/- 7.9 years in the control group, p = 0.33). In the PC group, blood was collected from the femoral vein through a 6F catheter introducer; 9 to 20 U (13.0 +/- 5.4 U, 0.42 +/- 0.22 U/kg) of autologous PC were prepared and were reinfused after protamine administration. The time course of platelet counts was examined until postoperative day 7. Aggregation responses to adenosine diphosphate; (4 micromol/L and 8 micromol/L), collagen (1 micromol/L and 5 micromol/L), and epinephrine (5 micromol/L and 10 micromol/L) were evaluated after induction of anesthesia (individual references), after protamine administration, at the end of the operation; these responses were shown as recovery ratios. RESULTS: Blood loss during surgery in the PC group was significantly less than in the control group (4.8 +/- 3.0 mL/kg versus 7.8 +/- 1.7 mL/kg, p = 0.044). Similarly blood loss on postoperative day 1 in the PC group was significantly less than in the control group (3.6 +/- 1.2 mL/kg versus 7.2 +/- 3.1 mL/kg, p = 0.013). The platelet counts in the PC group were larger than those in the control group until postoperative day 5, after reinfusion of prepared autologous PC. The recovery ratios of the aggregation responses to adenosine diphosphate, collagen, and epinephrine after protamine administration were not significantly different between the two groups. However, recovery in the PC group after reinfusion of the prepared autologous PC was greater than in the control group. CONCLUSIONS: Reinfusion of the freshly prepared autologous PC was followed by good aggregation responses and low blood loss in patients with noncyanotic congenital heart disease after open heart surgery. This procedure may be useful in pediatric open heart surgery without blood transfusion or with little administration of homologous blood products.

Adenosine Diphosphate↗
PubMed2000

Hemodynamic changes and right heart support during vertical displacement of the beating heart.

BACKGROUND: Hemodynamic instability during heart displacement in off-pump multivessel coronary artery bypass grafting might be related to right heart dysfunction. The Enabler (HemoDynamics Systems Ltd, Upper Yoqneam, Israel) is a cannula pump that expels blood from the right atrium into the pulmonary artery. We studied the hemodynamic changes and the role of the enabler during heart displacement. METHODS: Nine anesthetized sheep were assessed for hemodynamic changes during 90-degree heart displacement with or without Enabler support. Hemodynamic parameters included cardiac output, systemic arterial blood pressures, and left and right heart filling pressures. RESULTS: Heart displacement caused a significant decrease in cardiac output and systemic blood pressure (46%+/-5%, p = 0.001; and 20%+/-5%, p = 0.009, respectively), with a concomitant 137%+/-24% (p = 0.003) increase in central venous pressure. No significant change in left atrial pressure was observed. Activation of the Enabler caused a significant increase in cardiac output and systemic blood pressure (67%+/-15%, p = 0.01; and 17%+/-7%, p = 0.04, respectively), as well as a decrease in central venous pressure by 49%+/-8% (p = 0.0001). CONCLUSIONS: Heart displacement causes hemodynamic instability mainly by right heart dysfunction. The Enabler significantly stabilized circulation during vertical displacement of the beating heart.

Animals↗
PubMed1998

Non-uniform prolongation of intracellular Ca2+ transients recorded from the epicardial surface of isolated hearts from rabbits with heart failure.

OBJECTIVES: To study the time course of Ca2+ transients recorded from the left ventricular epicardial surface of isolated hearts from rabbits with heart failure and to correlate the results with mechanical function. METHODS: Heart failure was induced in the rabbit 8 weeks after coronary ligation (n = 17) with 13 controls. Echocardiography was used to assess in vivo left ventricular dysfunction. The fluorescent indicator Indo-1 was loaded into isolated Langendorff-perfused hearts and Ca2+ transients were recorded from 15 sites over the left ventricular epicardial surface using a single core light guide. The time course of the Ca2+ transients was analysed and the duration measured and correlated with in vitro mechanical function. RESULTS: Significant mechanical dysfunction was produced in this model of heart failure. The mean duration of the Ca2+ transients obtained from failing hearts was prolonged (156.2 +/- 3.2 ms) when compared to controls (124.9 +/- 2.6 ms, P < 0.001). Delayed relaxation as measured by the maximum rate of intraventricular pressure decay was significantly correlated with the prolonged Ca2+ transients (r = -0.63, P < 0.001). In addition, there was increased variation of the Ca2+ transient duration in the failing hearts. CONCLUSIONS: Coronary artery ligation-induced heart failure is associated with changes in the surviving myocardium which result in a non-uniform prolongation of Ca2+ transient duration. This suggests that there is a regional heterogeneity to the abnormal intracellular Ca2+ handling in heart failure.

Animals↗
PubMedDate not supplied

Severe depression is associated with markedly reduced heart rate variability in patients with stable coronary heart disease.

OBJECTIVE: The purpose of this study was to investigate the relationship between depression and heart rate variability in cardiac patients. METHODS: Heart rate variability was measured during 24-hour ambulatory electrocardiographic (ECG) monitoring in 40 medically stable out-patients with documented coronary heart disease meeting current diagnostic criteria for major depression, and 32 nondepressed, but otherwise comparable, patients. Patients discontinued beta-blockers and antidepressant medications at the time of study. Depressed patients were classified as mildly (n = 21) or moderately-to-severely depressed (n = 19) on the basis of Beck Depression Inventory scores. RESULTS: There were no significant differences among the groups in age, gender, blood pressure, history of myocardial infarction, diabetes, or smoking. Heart rates were higher and nearly all indices of heart rate variability were significantly reduced in the moderately-to-severely versus the nondepressed group. Heart rates were also higher and mean values for heart rate variability lower in the mildly depressed group compared with the nondepressed group, but these differences did not attain statistical significance. CONCLUSION: The association of moderate to severe depression with reduced heart rate variability in patients with stable coronary heart disease may reflect altered cardiac autonomic modulation and may explain their increased risk for mortality.

Aged↗
PubMed2003

Acellularized porcine heart valve scaffolds for heart valve tissue engineering and the risk of cross-species transmission of porcine endogenous retrovirus.

OBJECTIVE: Acellularized porcine heart valve scaffolds have been successfully used for heart valve tissue engineering, creating living functioning heart valve tissue. However, there is concern about the possibility of porcine endogenous retrovirus transmission. In this study we investigated whether acellularized porcine heart valve scaffold causes cross-species transmission of porcine endogenous retrovirus in a sheep model. METHODS: Acellularized porcine pulmonary valve conduits (n = 3) and in vitro autologous repopulated porcine pulmonary valve conduits (n = 5) were implanted into sheep in the pulmonary valve position. Surgery was carried out with cardiopulmonary bypass support. The animals were killed 6 months after the operation. Blood samples were collected regularly up to 6 months after the operation and tested for porcine endogenous retrovirus by means of polymerase chain reaction and reverse transcriptase-polymerase chain reaction. In addition, explanted tissue-engineered heart valves were tested for porcine endogenous retrovirus after 6 month in vivo. RESULTS: Porcine endogenous retrovirus DNA was detectable in acellularized porcine heart valve tissue. However, 6 months after implantation of in vitro and in vivo repopulated acellularized porcine heart valve scaffolds, no porcine endogenous retrovirus sequences were detectable in heart valve tissue and peripheral blood. CONCLUSION: Acellularized porcine matrix scaffolds used for creation of tissue-engineered heart valves do not transmit porcine endogenous retrovirus.

Animals↗
PubMed1999

Enkephalin inhibits vagal control of heart rate, contractile force and coronary blood flow in the canine heart in vivo.

The following studies were conducted to determine if the ability of the intrinsic cardiac opioid, met-enkephalin-arg-phe to interrupt vagal bradycardia can be generalized to include the disruption of vagal effects on atrial contraction and coronary blood flow. Anesthetized dogs were instrumented to measure heart rate and left atrial contractile force or heart rate and coronary blood flow. The response of each variable was recorded at rest and during vagal stimulation. During the evaluation of vagal effects on contractile activity and coronary blood flow, heart rate was maintained constant by electrically pacing the hearts above their resting heart rate. In the first protocol, vagal stimulation reduced both heart rate and atrial contractile force in a frequency dependent fashion. When met-enkephalin-arg-phe (MEAP) was infused systemically for three min at 3 nmol min(-1) kg(-1), there were no observed changes in resting heart rate or atrial contraction. However, when the vagal stimuli were reapplied during the peptide infusion, the previously observed vagal effects on rate and contractile force were reduced in magnitude by one-half to two-thirds. The ability of MEAP to interrupt the vagal control of heart rate and contractile activity involves opiate receptors since the effect was eliminated in both cases by prior opiate receptor blockade with the high affinity antagonist, diprenorphine. In the second protocol, vagal stimulation produced a transient increase in coronary blood flow and an accompanying increase in myocardial oxygen consumption. These effects were reduced by approximately 80% during the systemic infusion of MEAP. A similar increase in coronary blood flow mediated by the direct acting muscarinic agonist, methacholine, was unaltered by the infusion of peptide. In summary, these data suggest that the intrinsic cardiac enkephalin, MEAP, is capable of inhibiting the vagal control of heart rate, contractile force and coronary blood flow and probably does so through a common opiate receptor located prejunctionally on vagal nerve terminals or within nearby parasympathetic ganglia.

Adrenergic beta-Antagonists↗
PubMed2001

Influence of carvedilol on hospitalizations in heart failure: incidence, resource utilization and costs. U.S. Carvedilol Heart Failure Study Group.

BACKGROUND: Carvedilol reduces disease progression in heart failure, but to our knowledge, its effects on hospitalizations and costs have not been evaluated. OBJECTIVES: We examined the effects on hospitalization frequency and costs in the U.S. Carvedilol Heart Failure Trials Program. This program consisted of four concurrent, multicenter, double-blind, placebo-controlled studies involving 1,094 patients with New York Heart Association class II to IV heart failure, which treated patients with placebo or carvedilol for up to 15 months (median, 6.5 months). METHODS: Detailed resource utilization data were collected for all hospitalizations occurring between randomization and the end of follow-up. In-patient care costs were estimated based on observed levels of resource use. RESULTS: Compared with placebo, carvedilol reduced the risk of hospitalization for any reason by 29% (p = 0.009), cardiovascular hospitalizations by 28% (p = 0.034) and heart failure hospitalizations by 38% (p = 0.041). Carvedilol also decreased the mean number of hospitalizations per patient (for cardiovascular reasons 30% [p = 0.02], for heart failure 53% [p = 0.03]). Among hospitalized patients, carvedilol reduced severity of illness during hospital admission, as reflected by shorter length of stay and less frequent use of intensive care. For heart failure hospital admissions, carvedilol decreased mean length of stay by 37% (p = 0.03) and mean number of intensive care unit/coronary care unit days by 83% (p = 0.001), with similar effects on cardiovascular admissions. As a result, estimated inpatient care costs with carvedilol were 57% lower for cardiovascular admissions (p = 0.016) and 81% lower for heart failure admissions (p = 0.022). CONCLUSIONS: Carvedilol added to angiotensin-converting enzyme inhibition reduces hospitalization risk as well as severity of illness and resource utilization during admission in patients with chronic heart failure.

Adrenergic beta-Antagonists↗
PubMed1996

Prognostic value of heart rate variability during long-term follow-up in patients with mild to moderate heart failure. The Dutch Ibopamine Multicenter Trial Study Group.

OBJECTIVES: We sought to assess the prognostic value of heart rate variability measures, including Poincaré plots, in patients with mild to moderate chronic heart failure. BACKGROUND: Mortality is high in patients with heart failure, and many of them die suddenly. However, identification of high risk patients, particularly those with an increased risk for sudden death, has remained difficult. METHODS: We studied 95 patients with heart failure (mean [+/- SD] age 60 +/- 8 years, left ventricular ejection fraction 0.29 +/- 0.09, New York Heart Association functional class II [81%] and III [19%]) during up to 4 years of follow-up. Heart rate variability measures and Poincaré plots were obtained from 24-h Holter recordings. RESULTS: During follow-up, 17 (18%) of the 95 patients died. In 15 patients, death was cardiac related (11 patients experienced sudden death). None of the conventional time and frequency domain measures of heart rate variability were related to survival. In contrast, abnormal Poincaré plots identified a significantly higher risk for all-cause cardiac death (Cox proportional hazards ratio 5.7, 95% confidence interval [CI] 1.6 to 20.6, univariate analysis) and for sudden cardiac death (hazards ratio 6.8, 95% CI 1.5 to 31.4) compared with those with normal Poincaré plots. Patients with abnormal Poincaré plots were shown to have a lower left ventricular ejection fraction (0.26 +/- 0.10 vs. 0.31 +/- 0.08, p < 0.05) and higher plasma norepinephrine concentrations (506 +/- 207 pg/ml vs. 411 +/- 175 pg/ml, p < 0.05). In multivariate analysis, abnormal Poincaré plots still had independent prognostic value, both for all-cause cardiac mortality and for sudden cardiac death (hazards ratio 5.3, 95% CI 1.2 to 17.1, hazards ratio 4.5, 95% CI 1.0 to 27.5, respectively. CONCLUSIONS: Heart rate variability analysis, as assessed by Poincaré plots, has independent prognostic value in patients with mild to moderate chronic heart failure and identifies an increased risk for all-cause and sudden cardiac death in these patients.

Adolescent↗
PubMed2000

Expression of proinflammatory cytokines in the failing human heart: comparison of recent-onset and end-stage congestive heart failure.

BACKGROUND: Plasma levels of proinflammatory cytokines, including tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, are elevated in patients with congestive heart failure (CHF). Recent studies suggest that the failing human heart is a source of proinflammatory cytokines in the end-stage failing heart. However, the relevance of plasma levels to those of the myocardium remains undefined. We sought to compare cytokine expression in early and end-stage CHF, and to evaluate the correlation of tissue expression to plasma levels. METHODS: Two patient populations were studied: patients with recent-onset CHF, all with symptoms less than 6 months (n = 17, duration of symptoms 2.1 +/- 1.6 months, range of New York Heart Association (NYHA) 1 to 3), and end-stage heart-failure patients (n = 7) who underwent left-ventricular assist-device (LVAD) implantation (Duration of symptoms 47.1 +/- 28.0 months, all NYHA class 4). Plasma levels of TNF-alpha and IL-6 proteins were evaluated by an Enzyme-Linked Immuno-Sorbent Assay (ELISA), while myocardial levels of cytokine transcripts were assessed by ribonuclease (Rnase) protection assay. RESULTS: In patients with end-stage heart failure, TNF-alpha and IL-6 were increased in the plasma as well as in the myocardium (plasma: TNF-alpha = 7.7 +/- 2.3 pg/ml, IL-6 = 45.0 +/- 47.1 pg/ml; myocardium: TNF-alpha = 0.31 +/- 0.15% of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression, IL-6 = 1.56 +/- 1.54% ). In contrast, despite elevated plasma levels of TNF-alpha and IL-6, the myocardium of patients with the recent onset of symptoms demonstrated minimal expression of TNF-alpha and IL-6 messenger ribonucleic acid (mRNA) (plasma: TNF-alpha = 4.3 +/- 1.7 pg/ml, IL-6 = 3.3 +/- 1.8 pg/ml; myocardium: TNF-alpha = 0.13 +/- 0. 04%, IL-6 = 0.02 +/- 0.04%). Plasma levels of TNF-alpha were significantly correlated with those in the myocardium when both populations were combined. (r = 0.69, p < 0.001). CONCLUSIONS: Cytokines are expressed in the myocardium in end-stage heart failure to a much greater degree than in patients with the recent-onset of symptoms. This suggests that induction of cytokines in the myocardium is a relatively late event in the pathogenesis of CHF. Furthermore, plasma levels of TNF-alpha correlates with mRNA expression in the myocardium and thus may serve as an appropriate marker of myocardial cytokine activation. Whether the production of cytokines in the failing human heart precedes the elevation of cytokines in the plasma remains undefined. Therefore, we studied expression of TNF-alpha and IL-6 in the myocardium as well as in the plasma in patients with early and end-stage CHF. The results have demonstrated that cytokines are expressed in the myocardium in end-stage heart failure to a much greater degree than in patients with the recent onset of symptoms. This suggests that induction of cytokines in the myocardium is a relatively late event in the pathogenesis of CHF.

Adult↗
PubMed2000

A Rapid Access Heart Failure Clinic provides a prompt diagnosis and appropriate management of new heart failure presenting in the community.

BACKGROUND AND AIMS: The diagnosis of heart failure is an important clinical problem and yet reported diagnostic accuracy in primary care is less than 50%. We established a Rapid Access Heart Failure Clinic (RAHFC) in a district general hospital serving a population of 292,000 in SE London, UK, to diagnose and manage new cases of heart failure presenting for the first time in the community. METHODS: Patients with suspected new onset heart failure were referred by their Primary Care Physician without appointment for clinical assessment on the same or next working day. Assessment by a specialist registrar in cardiology included history, examination, chest X-ray, electrocardiogram (ECG) and echocardiogram. When a diagnosis of heart failure was made appropriate treatment, including angiotensin converting enzyme inhibitors (ACEI), was started. RESULTS: Over 15 months 383 patients were seen (0.4 cases/100,000 population/weekday) 178/383 (46%) were considered to have definite or possible heart failure at the initial assessment in the RAHFC. A normal ECG (negative predictive value 94%) and chest X-ray virtually excluded the diagnosis of heart failure. After subsequent specialist investigations and follow-up, including a trial of therapy where appropriate, 101/383 (26%) were finally diagnosed as clinical heart failure. ACEI therapy was commenced in 56/57 (98%) of patients in whom it was considered appropriate. CONCLUSION: The RAHFC provided rapid assessment, prompt diagnosis and early introduction of life prolonging therapy for patients presenting with suspected heart failure in the community.

Aged↗
PubMed1997

Classification of heart failure in population based research: an assessment of six heart failure scores.

Several scores based on symptoms and signs have been developed to assess the presence of heart failure. The goal of this study was to compare six heart failure scores in non-hospitalised subjects and to determine their usefulness in population based research. The scores were applied to 54 participants of a population based study. All underwent a complete medical examination, including chest X-ray, electrocardiography and Doppler echocardiography. Using all information available, a cardiologist, unaware of the results of the scores, clinically classified participants as having no, possible or definite heart failure. Sensitivity, specificity, predictive values and receiver operating characteristics were calculated, using the cardiologist's assessment as a gold standard. The cardiologist judged definite or possible heart failure to be present in 17 persons. All scores had a high sensitivity for the detection of definite heart failure, whereas the study of men born in 1913 and Walma's score had the highest sensitivity for the combination of possible and definite heart failure. Gheorgiade's and the Boston score had the highest positive predictive values. In conclusion, five of the six scores we studied are broadly similar in the detection of heart failure. The men born in 1913 score relies heavily on the assessment of dyspnea, resulting in a relatively large number of false positives. Although the scores are useful in detecting manifest heart failure, objective measurements of cardiac function appear necessary to reduce the false positive rate and accurately detect early stages of heart failure.

Aged↗
PubMed2000

An examination of the relationship between resting heart rate variability and heart rate reactivity to a mental arithmetic stressor.

Resting heart rate variability can be an index of sympathetic or parasympathetic dominance, according to the frequency of the variability studied. Sympathetic dominance of this system has been linked to increased risk of cardiovascular disease (CVD). Similarly, rapid and dramatic increases in heart rate reactivity to a stressor task have also been suggested as indicating increased risk of CVD via atherogenesis. Although both of these variables have been related to the development of cardiovascular disease, and both may be related to increased sympathetic activity or parasympathetic withdrawal, most research studies have tended to focus on either variable independently of the other. In order to investigate whether these two indices of stressor reactivity were related in relatively young and healthy subjects, resting heart rate variability data were collected from 80 volunteers for 20 minutes. In addition, heart rate reactivity data were collected during a 2-minute mental arithmetic stressor, which has been previously shown to induce significant increases in heart rate. After classifying subjects according to whether their heart rate variability data were above or below the mean for their gender, heart rate reactivity data were examined via MANOVA to detect significant differences between subject groups. Females showed significant effects, and males showed nonsignificant trends, but these two sets of data were in different directions, suggesting that gender may be a confounding factor in the relationship between heart rate reactivity and heart rate variability.

Adolescent↗
PubMed1980

Differences in the metabolism of very-low-density lipoproteins by isolated beating-heart cells and the isolated perfused rat heart. Evidence for collagenase-released extracellular lipoprotein lipase.

1. The metabolism of VLD lipoproteins (very-low-density lipoproteins) was studied in intact isolated beating-heart cells and isolated perfused rat heart from starved animals by using [14C]triacylglycerol fatty acid-labelled VLD lipoprotein prepared from rats previously injected with [1-14C]palmitate. 2. 14C-labelled VLD lipoprotein was metabolized by the isolated perfused heart, but was only minimally metabolized by the heart cells unless an exogenous source of lipoprotein lipase was added. 3. Measurements of lipoprotein lipase at pH 7.4 with the natural substrate 14C-labelled VLD lipoprotein indicated that during collagenase perfusion of the heart the enzyme was released into the perfusate, the activity released being proportional to the concentration of collagenase used. Lipoprotein lipase activity in homogenates of hearts that had been perfused with collagenase showed a corresponding loss of activity. 4. At high perfusate concentrations of collagenase, inactivation of the released lipoprotein lipase occurred. 5. Lipoprotein lipase activity was largely undetectable in the homogenate of the isolated heart cells. 6. It is concluded that the lipoprotein lipase responsible for the hydrolysis of VLD lipoprotein triacylglycerol is predominantly located externally to the heart muscle cells and that its release can be facilitated by perfusion of the heart with bacterial collagenase.

Animals↗
PubMed1993

Pyrophosphate metabolism in the perfused heart and isolated heart mitochondria and its role in regulation of mitochondrial function by calcium.

1. Langendorff-perfused rat hearts were treated, either alone or in combination, with acetate, adrenaline or supraphysiological [Ca2+] to mimic increased workload. No significant increases in the PPi content of the freeze-clamped tissue were observed. 2. In contrast with liver mitochondria, isolated rat heart mitochondria incubated at a free [Mg2+] of 1.5 mM showed little or no increase in matrix PPi content or volume in the presence of 0.75 microM Ca2+; neither did 5 mM acetate cause heart mitochondrial PPi to increase. 3. At 0.1 mM Mg2+ some increase in matrix PPi content of heart mitochondria was observed, and increases in liver mitochondria were significantly greater. 4. Substantial increases in heart mitochondrial-matrix PPi content were observed at 1.5 mM Mg2+ when [Ca2+] > 1 microM, especially in the presence of acetate, or at 0.75 microM Ca2+ in the presence of bongkrekic acid to inhibit the adenine nucleotide translocase. 5. Total pyrophosphatase activity was similar in heart and liver mitochondrial matrix extract and toluene-permeabilized mitochondria. 6. These data suggest that under physiological conditions Ca2+ does not regulate heart mitochondrial [PPi], because higher matrix [Mg2+] overcomes the inhibition of pyrophosphatase by Ca2+, and also significant loss of PPi from the matrix on the adenine nucleotide translocase may occur. 7. It is concluded that, in contrast with the situation in liver [Halestrap (1989) Biochim. Biophys. Acta 973, 355-382], Ca(2+)-induced PPi-mediated increases in mitochondrial volume are unlikely to play a physiological role in the heart. 8. The substantial swelling of liver and kidney mitochondria caused by addition of supraphysiological [Ca2+] (20 nmol/mg of protein) was associated with significant increases in PPi content, but was not observed in heart mitochondria. 9. This substantiates the role that we have proposed for PPi in the opening of a non-specific pore by Ca2+ overload of mitochondria [Halestrap and Davidson (1990) Biochem. J. 268, 153-160].

Animals↗
PubMed2002

Median maximal heart rate for heart rate calibration in different conditions: laboratory, field and competition.

The objective of this study was to evaluate the variability of maximal heart rate in three different conditions: laboratory tests, field tests, and competitions. Sixteen male endurance volunteers were tested in five exhaustive tests for each condition. All exhaustive events were heart rate monitored (Accurex plus, Polar Electro, Finland) and true maximal heart rates were assessed and compared with each other and with predicted maximal heart rates. Results show that under the three conditions HR(peaks) were not statistically different (p = 0.62, NS, Friedman test). Mean HR(peaks) (SD) were: laboratory = 194.3 (7.8), field = 193.8 (11.8), competition = 192.3 (10.1) beats x min(-1). Conditions for reaching individual heart rate peak were in the laboratory (treadmill VO(2)max protocol) for 5 subjects, in field tests for 7 subjects and in competitions for 6 subjects (two circumstances for two subjects). A large intra-individual variation existed in the three circumstances (+/- 6 beats x min(-1)). Absolute median maximal heart rate was 190.0 bpm (9.32) i.e 7.6 bpm lower than heart rate peak. Both were highly related (rho = 0.89, z = 3.449, p = 0.0006, Spearman test). Median maximal heart rates inter-condition relationship were higher. Median maximal heart rate was more stable and took more information into account than an isolated peak. It gives a central value that minimizes the potential risk of under or over estimation when calibrating exercise intensities with HR.

Adult↗
PubMed2002

Long-term outcome and the use of revascularization in patients with heart failure, suspected ischemic heart disease, and large reversible myocardial perfusion defects.

BACKGROUND: The potential role of coronary revascularization in the management of patients with congestive heart failure and suspected ischemic heart disease remains to be defined. Myocardial perfusion imaging can identify patients with ischemic heart disease as the etiology for left ventricular dysfunction who might benefit from revascularization. METHODS: We retrospectively identified heart failure patients with suspected ischemic heart disease who had large reversible perfusion defects to determine their long-term outcome and rate of revascularization. The study group consisted of 77 patients with congestive heart failure, left ventricular ejection fraction <45%, and suspected ischemic heart disease who underwent myocardial perfusion imaging during the period of January 1, 1991, to December 31, 1997, and had large reversible perfusion defects. RESULTS: The 5-year mortality rate was 57.6%. The revascularization rate was only 13% for 5 years of follow-up. The number of patients undergoing revascularization was too small to assess its impact on outcome. CONCLUSION: These results indicate a high 5-year mortality rate and a low utilization of coronary revascularization in patients with heart failure and large reversible perfusion defects. The low rate of revascularization reflects at least in part the absence of the generalizability of the existing literature to the optimal means of treating patients with heart failure and myocardial ischemia and points to the need for a randomized clinical trial.

Aged↗