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PubMed2005

Cardiothoracic surgery after heart and heart-lung transplantation.

OBJECTIVE: We sought to examine our management and the outcomes of cardiothoracic procedures after heart and heart lung transplantation. METHODS: We performed a retrospective review of cardiothoracic surgical procedures carried out between 1990 and 2004 in patients who had previously undergone heart or heart-lung transplantation at our institution. RESULTS: Twenty-one out of 340 patients (6.2 %) were identified. Cardiothoracic surgery was performed 44.4 +/- 33 months (range 1 - 115 months) after transplantation. Predominant types of surgery were coronary artery bypass grafting due to allograft vasculopathy (n = 5), aortic surgery due to acute dissection (n = 3), biventricular assist device implantation due to acute rejection (n = 1), tricuspid valve repair (n = 1), multiple cardiac surgical procedures including coronary artery bypass grafting, retransplantation, and tricuspid valve replacement (n = 2), explantation of a functionless heterotopic transplanted heart (n = 1). Lung surgery was performed in six patients due to pneumonia (n = 2), primary lung carcinoma (n = 3), lung torsion following heart-lung transplantation (n = 1). All patients underwent either lobectomy or segmental lung resection. Single lung retransplantation (n = 2) after prior heart-lung transplantation due to bronchiolitis obliterans was performed. In one patient a pneumonectomy (n = 1) due to severe chronic rejection of the contralateral lung was performed. Six subsequent deaths after cardiothoracic procedures were recorded after 1, 4, 78, 163, 205, and 730 days, respectively. Causes of death were advanced carcinoma (n = 1), multi-organ failure due to sepsis (n = 2), sudden heart death (n = 2), and advanced heart failure (n = 1). Fifteen out of 21 patients having undergone cardiothoracic procedures (71.4 %) survived the observation period of 56.6 +/- 34 months (range 1 - 114). CONCLUSIONS: Reasons for cardiothoracic procedures after prior heart or heart-lung transplantation were allograft vasculopathy, aortic dissections years after transplantation, chronic rejection, and either lung infections or malignancies. Surgical repair can be performed with an acceptable operative risk and good long-term survival rates.

Cardiac Surgical Procedures↗
PubMedDate not supplied

Beta-blocker therapy for heart failure: should the therapeutic target be dose or heart rate reduction?

Therapeutic target with beta blockers in heart failure, i.e., target heart rate reduction or beta-blocker dose, is controversial. To resolve this controversy, the authors studied 152 heart failure patients on beta blockers who were divided into four groups based on median peak exercise heart rate reduction as compared with predicted and prescription of at least 50% recommended beta-blocker dose. Event-free survival (vs. death or assist device placement or urgent transplantation) was compared. Baseline and peak exercise heart rates were 74 +/- 14 and 116 +/- 21 bpm, respectively. Median heart rate reduction at peak exercise was 35%. When median or higher peak heart rate reduction was achieved, there were no significant survival differences noted between patients on different beta-blocker doses. With below-median peak heart rate reduction, there was a strong trend toward better event-free survival with higher beta-blocker doses. In conclusion, the results suggest that higher heart rate reduction is associated with better outcomes for heart failure patients overall and, for patients with persistently elevated heart rates, higher beta-blocker doses provided additional benefit.

Adrenergic beta-Antagonists↗
PubMed1994

Heart rate variability in left ventricular dysfunction and heart failure: effects and implications of drug treatment.

OBJECTIVE: To review the importance of heart rate variability analysis in left ventricular dysfunction and heart failure and to assess the effects of drug treatment. In patients with left ventricular dysfunction or heart failure, a low heart rate variability is a strong predictor of a low probability of survival. Because drug treatment in these patients has rapidly changed over the past two decades, the effect of these drugs on heart rate variability needs special attention. DESIGN: A study of published reports to give an overview of heart rate variability in patients with left ventricular dysfunction or heart failure and how it is affected by drug treatment. RESULTS: Analysis of heart rate variability provides an easily obtained early marker for progression of disease. It seems to be more closely related to the degree of neurohumoral activation than to haemodynamic variables. Cardiovascular drugs may either stimulate or inhibit the degree of neurohumoral activation, and the effects of pharmacological intervention can be closely monitored with this method. CONCLUSIONS: The analysis of heart rate variability, including spectral analysis, is a novel non-invasive way to obtain potentially useful clinical information in patients with reduced left ventricular function. The effects of drug treatment on heart rate variability are in general consistent with their long-term effects in left ventricular dysfunction and heart failure.

Heart Failure↗
PubMedDate not supplied

Gene expression of antioxidative enzymes in the human heart: increased expression of catalase in the end-stage failing heart.

BACKGROUND: An increase in oxidative stress is suggested to be intimately involved in the pathogenesis of heart failure. However, gene expression of enzymes that metabolize reactive oxygen metabolites has not been investigated in the human heart. METHODS AND RESULTS: Myocardial tissue homogenates of the left ventricular wall from hearts in end-stage failure due to dilated (DCM) or ischemic (ICM) cardiomyopathy (n=12 each), as well as from nonfailing donor hearts (n=12), were analyzed for mRNA levels of manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), glutathione peroxidase (GPX), and catalase by Northern blot analyses. Protein levels of MnSOD, CuZnSOD, and catalase were determined by Western blot or ELISA. MnSOD, CuZnSOD, and GPX mRNA levels were similar in all 3 groups. In contrast, catalase mRNA levels were found to be increased by 123+/-23% in DCM hearts and by 93+/-10% in ICM hearts (P<0.01 each) compared with control hearts. Likewise, catalase protein levels were found to be increased in failing hearts (DCM by 90+/-10%, ICM by 90+/-13%; P<0. 05 each) compared with control hearts. In addition, the observed upregulation of catalase mRNA and protein in failing hearts was attended by an increased catalase enzyme activity (DCM by 124+/-16%, ICM by 117+/-15%; P<0.01 each), whereas MnSOD, CuZnSOD, and GPX enzyme activity levels were unchanged in failing compared with nonfailing myocardium. CONCLUSIONS: Increased oxidative stress in human end-stage heart failure may result in a specific upregulation of catalase gene expression as a compensatory mechanism, whereas SOD and GPX gene expression remain unaffected.

Adult↗
PubMed1987

Right heart pressure does not equal pericardial pressure in the potassium chloride-arrested canine heart in situ.

Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.

Animals↗
PubMed1995

Importance of initial coronary artery flow after heart procurement to assess heart viability before transplantation.

BACKGROUND: The objective of this study was to evaluate different tests of heart viability in a pig model of warm ischemia. METHODS AND RESULTS: Pig hearts (n = 30) were submitted to 0 (= group I), 10 (group II), 20 (group III), 30 (group IV), and 60 (group V) minutes of in situ warm ischemia (animal exsanguination). Hearts were removed, then flushed with cardioplegic solution for 3 minutes at a fixed pressure of 60 cm H2O, and edema formation, initial coronary flow, and ionic composition (Na+, K+, and Ca++) of coronary sinus effluent were evaluated. Hearts were then stored for 2 hours in a cold (4 degrees C) preservation solution. Myocardial biopsies (and evaluation of energetic index) were performed, then the hearts were reperfused for 30 minutes with whole blood with an in vitro functional testing system. No edema occurred during cardioplegic flush in the hearts in groups I through IV, but a 37 +/- 11% weight increase (P < .001) occurred in hearts in group V. There was a progressive decrease in initial coronary flow with the increase in the duration of warm ischemia (70 +/- 14 mL/min per 100 g of tissue in group I and 52 +/- 9, 41 +/- 16, 25 +/- 11, and 23 +/- 5 mL/min per 100 g, respectively, in groups II through V (P < .01 to P < .001 versus group I). Initial coronary flow was positively correlated with the energetic index (r = .84, P < .001), and the left ventricle developed pressure at reperfusion (r = .90, P < .001). Finally, there were significant differences between hearts in the control group and those in group V for calcium and sodium release (lower in the control group; P < .001 and P < .01, respectively) and for potassium removal (lower in group V, P < .05). CONCLUSIONS: These data suggest that early measurement of coronary flow after removal of the heart may help to assess heart viability before transplantation. This approach may provide a comprehensive clinical evaluation to increase the number of hearts available for transplantation among those that are rejected in the absence of accurate criteria of viability.

Animals↗
PubMed2006

Long-term effects of cardiac resynchronization therapy on heart rate and heart rate variability.

Congestive heart failure is characterized by significant autonomic dysfunction. Development of left bundle branch block in congestive heart failure is a predictor of worse outcome. There are several lines of evidence that cardiac resynchronization therapy (CRT), by biventricular stimulation in patients with severe heart failure and left bundle branch block, improves autonomic functions which can be quantified by measuring heart rate variability. The aim of the present study was to assess the effect of CRT on autonomic functions quantified by heart rate variability and mean heart rate (HR) in patients with advanced heart failure and left bundle branch block in short and long-term follow-up. A total of 35 patients with systolic heart failure and left bundle branch block (mean-age 60 +/- 11 years; 24 male and 11 female; mean left ventricular ejection fraction [EF]: 22.3 +/- 3%) were enrolled. Clinical assessment and echocardiographic examination were performed at baseline and every three months. Continuous electrocardiographic monitorization by 24-hour Holter recordings was performed pre-implantation, 3 months and 2 years after implantation. Mean HR and one of the time-domain parameters of heart rate variability, standard deviation of the R-R intervals (SDNN) were measured. CRT was associated with a decrease in the mean duration of QRS, and an increase in diastolic filling time, the rate with which the left ventricular pressure rises (dP/dt), and left ventricular ejection fraction. Decrease in mean heart rate and increase in SDNN were statistically significant in the third month and second year recordings when compared to baseline recording (p values were < 0.001 for both). In conclusion, CRT with biventricular pacing provides sustained improvement in autonomic function in patients with advanced heart failure and left bundle branch block.

Female↗
PubMedDate not supplied

[From ischaemia to heart failure: heart rate--actor or stamper?].

The heart rate in sinus rhythm depends on If current-induced automaticity of sinus node cells. Such a current is activated by hyperpolarisation and is modulated by influences from sympathetic and para-sympathetic tones. There are established prognostic values for the baseline heart rate and its variability in coronary heart disease and heart failure. However, heart rate per se directly modulates myocardial oxygen consumption and cardiac contractility by interfering with the excitation-contraction coupling. The therapeutic implications of pharmacological modulation of the heart rate are important mainly for slowing the heart rate, as illustrated by the use of calcium antagonists in coronary heart disease and beta-blockers in both coronary heart disease and heart failure. The possibility of a direct action on sinusal automaticity by drugs such as ivabradine, an If channel blocker, reveals new therapeutic perspectives. Indeed, a benefit of combination therapy with these drugs and beta-blockers should be lower heart rate values than can be attained with maximally tolerated doses of beta-blockers.

Autonomic Nervous System↗
PubMed2002

[Adaptation of guidelines for the treatment of chronic heart failure in a specialized heart failure clinic].

BACKGROUND: Chronic heart failure is associated with high mortality and morbidity. In spite of a number of trials showing significant improvement in survival and reduction in hospitalization for patients who received ACE inhibitors/AT1 receptor antagonists (ACEI/ARB), beta-blockers and spironolactone, and notwithstanding the recommendations of national and international guidelines for the management of heart failure, substantial proportions of patients are not receiving this treatment. The aim of our study was to analyse 1. the efficiency of a specialized heart failure clinic in translating guidelines into clinical practice, and 2. the effect of optimized neurohormonal therapy on patient outcome. METHODS AND RESULTS: The data of patients with systolic heart failure and an ejection fraction < or = 35% referred to the Innsbruck Heart Failure and Transplantation Program between February 2000 and October 2001 were analysed. The number of patients treated with ACEI/ARB, beta-blocker and spironolactone increased significantly in the investigation period (p < 0.05). Equivalent dose for captopril and bisoprolol per patient developed from 66.4 +/- 42.8 to 96.5 +/- 41.9 mg (p < 0.001) and from 2.0 +/- 2.9 to 6.3 +/- 4.0 mg (p < 0.001), respectively. Optimization of neurohormonal therapy was associated with a significant improvement in NYHA class (2.5 +/- 0.8 vs. 1.9 +/- 0.8; p < 0.001). No relevant changes were noticed for blood pressure, serum creatinine, serum sodium, and serum potassium, whereas heart rate dropped significantly. Kaplan-Meier curves examining the time to first event of the combined end point of mortality and hospitalisation for worsening heart failure revealed a clear benefit for patients on combined neurohormonal therapy (ACEI/ARB and beta-blocker, n = 86) when compared with patients on neurohormonal monotherapy (ACEI/ARB or beta-blocker, n = 35), (p < or = 0.001). Differences remained significant (p = 0.022) after adjusting for NYHA class at referral, age, gender, etiology of the underlying cardiomyopathy, ejection fraction, and atrial fibrillation in Cox regression analysis. CONCLUSION: Guidelines for the management of chronic heart failure patients can be translated efficiently into clinical practice by a specialized heart failure clinic. Optimization of therapy is associated with an improvement in functional status and a decrease in mortality or hospitalization for worsening heart failure. Therefore the nationwide installation of specialized heart failure clinics is required.

Adrenergic beta-Antagonists↗
PubMed1990

Effects of left heart bypass on right ventricular performance. Evaluation of the right ventricular end-systolic and end-diastolic pressure-volume relation in the in situ normal canine heart.

Although left heart bypass has gained popularity as a powerful technique to assist the severely failed left heart, apparent right heart failure has often developed during the bypass procedure. We investigated whether the coexisting right heart failure is attributable to the left heart bypass in 16 open-chest dogs. We evaluated the effects of left heart bypass on the right ventricular systolic properties by the slope of the end-systolic pressure-volume relation and its effects on the diastolic properties by chamber compliance. Overall right ventricular performance was assessed by the end-diastolic pressure versus cardiac output relationship. The left heart bypass decreased the slope slightly when the assisted flow ratio exceeded 75% (-14% +/- 8% at the assisted flow ratio of 100%, p less than 0.02) and thus had a deleterious influence on right ventricular performance. The left heart bypass, on the other hand, had a counteracting beneficial influence on right ventricular performance through the increase in chamber compliance (38% +/- 5%, p less than 0.01) and the decrease in pulmonary arterial input resistance (-15% +/- 12%, p less than 0.01). The net effect of the left heart bypass was the increase in cardiac output (20% +/- 2%, p less than 0.05) for any given right ventricular end-diastolic pressure. We conclude that in normal hearts the left heart bypass augments right ventricular performance. We ascribe these beneficial effects to diastolic ventricular interdependence and afterload unloading.

Animals↗
PubMed1989

Heart and heart-lung transplantation, Papworth Hospital, 1979-1989.

The quality of life for those who survive the first 3 months after transplantation is generally good (10). The duration of hospital stay and the cost of transplantation per patient has been reduced during the last 3 years. Cardiologists are coming to appreciate the therapeutic potential of both heart and heart-lung transplantation. One of the chief logistical problems now being faced is that of increasing the provision of transplant services to match the increasing demand. It was said in an earlier edition of this book that this would be donor organ limited and that pattern already seen in the United States is becoming apparent in the United Kingdom. The broad principles of management of heart and heart-lung recipients have been established. Further improvements in medium and long-term results can be anticipated as a result of refining immunosuppression and defining the cause of chronic donor organ related damage (small vessel coronary occlusive disease in heart transplants and chronic obliterative bronchiolitis in heart-lung transplants). Heart transplantation has become firmly established as a therapeutic option for life threatening heart disease. It is probably too early to attribute this label to heart-lung transplantation which continues through its developmental phase with acceptable short-term results. Improvements in chronic damage characteristic of long-term survival in both heart and heart-lung transplant recipients will be a significant clinical step forward in this field.

Adolescent↗
PubMed1997

Restrictive criteria for heart transplantation candidacy maximize survival of patients with advanced heart failure.

BACKGROUND: The shortage of organ donors and the amelioration of medical management of advanced heart failure mandate strict selection of heart transplant candidates on the basis of the need and probability of success of transplantation, with the aim of maximizing survival of patients with advanced heart failure, both with and without transplantation. This study analyzes the impact of restricting the criteria for heart transplantation candidacy on the outcome of patients with advanced heart failure referred for transplantation. METHODS: Survival and freedom from major cardiac events (death, resuscitated cardiac arrest, transplantation while supported with inotropes or mechanical devices) were compared between patients listed during 1990 to 1991, when standard criteria were applied (group 1, n = 118), and patients listed during 1993 to 1994, when only patients requiring continuous/recurrent intravenous inotrope therapy in spite of optimized oral medications and outpatients showing actual progression of the disease were admitted to the waiting list (group 2, n = 88). Survival and freedom from cardiac events (defined as above plus listing in urgent status) were also calculated in stable outpatients evaluated in 1993 to 1994, who were potential heart transplant candidates according to standard criteria but were not listed because of restrictive criteria (group 3, n = 52, New York Heart Association functional class > or = III, mean echocardiographic ejection fraction 0.22 +/- 0.05, mean peak oxygen consumption 12.3 +/- 1.5 ml/kg/min, mean follow-up 19 +/- 10 months). RESULTS: Thirty-one percent, 40%, and 50% of group 1 patients versus 58%, 65%, and 77% of group 2 patients underwent transplantation within 3, 6, and 12 months after listing (p < 0.0007). The 1- and 2-year survival rates after listing were 80% and 71% in group 1 versus 85% and 84% in group 2 (p < 0.0001). Freedom from death/urgent transplantation was lower in group 2 than in group 1 (55% and 48% versus 72% and 59% at 6 and 12 months, respectively; p < 0.0001). In patients undergoing transplantation, the postoperative survival rate was similar (87% and 91% at 2 years in group 1 and group 2, respectively). Two years after heart transplantation candidacy was denied, 86% of group 3 patients were alive, and 74% were event-free. CONCLUSIONS: Restricting the admissions to the waiting list to patients with refractory/progressive heart failure improved survival rates after listing by increasing the probability to undergo transplantation in a short time. Selection of most severely ill candidates did not affect postoperative survival. Survival and freedom from cardiac events were good in patients with advanced but stable heart failure, in spite of their severe functional limitation. Thus restrictive criteria for heart transplantation candidacy allows maximal survival benefit from both medical therapy and transplantation.

Adolescent↗
PubMed1975

Hemodynamic changes during ventricular pacing in patients with complete heart block and aortic and mitral valvular heart disease.

Increasing the heart rate to near normal in patients with complete heart block (CHB) and slow ventricular rates may lead to greater improvement in ventricular function than when the heart rate is increased from normal to more rapid heart rates. Improvement in ventricular function is usually manifested by a decrease in left ventricular end-diastolic pressure (LVEDP) and volume and by an increase in contractility. In patients with both CHB and valvular heart disease improvement in ventricular function during pacing may be modified by the nature of the valvular disease. Hemodynamic data from six patients with both valvular heart disease and CHB were compared with those from ten patients with CHB and normal cardiac valves. Hemodynamic studies were performed at slow or idioventricular rates and again after increasing the heart rate to more nearly normal levels by ventricular pacing. When obstruction to left ventricular inflow (mitral stenosis) co-existed with CHB, increasing the heart rate resulted in a reduction of an elevated LVEDP to normal. This resulted in only a small increase in left atrial pressure in spite of a striking increase in the mean left atrial-ventricular gradient. When obstruction to left ventricular outflow prevailed (aortic stenosis), improvement in cardiac function was manifested mainly by a decrease in LVEDP and was accompanied by a decrease in left ventricular stroke work. When a large regurgitant volume (aortic insufficiency) was added to a ventricle which has enlarged subsequent to CHB, there was striking elevation in ventricular filling pressures which returned to more nearly normal levels when the heart rate was increased. This was accompanied by a reduction in regurgitant stroke volume in the patient in whom it was measured. Thus, an increase in heart rate may be especially beneficial to those patients with CHB who also have valvular lesions which contribute to an increase in LVEDP and end-diastolic volume. Careful hemodynamic evaluation is helpful in determining appropriate therapy in these patients.

Aged↗
PubMed1996

Heart rate variability in isolated rabbit hearts.

The presence of heart rate variability (HRV) in patients with cardiac denervation after heart transplantation raised our interest in HRV of isolated, denervated hearts. Hearts from seven adult white ELCO rabbits were transferred to a perfusion apparatus. All hearts were perfused in the working mode and in the Langendorff mode for 20 minutes each. HRV was analyzed in the frequency domain. A computer simulated test ECG at a constant rate of 2 Hz was used for error estimation of the system. In the isolated, denervated heart, HRV was of random, broadband fluctuations, different from the well-characterized oscillations at specific frequencies in intact animals. Mean NN was 423 +/- 51 ms in the Langendorff mode, 406 +/- 33 ms in the working heart mode, and 500 ms in the test ECG. Total power was 663 +/- 207 ms2, 817 +/- 318 ms2, and 3.7 ms2, respectively. There was no significant difference in any measure of HRV between Langendorff and working heart modes. The data provide evidence for the presence of HRV in isolated, denervated rabbit hearts. Left atrial and ventricular filling, i.e., the working heart mode, did not alter HRV, indicating that left atrial or ventricular stretch did not influence the sinus nodal discharge rate.

Animals↗
PubMed2002

Association of nonsteroidal anti-inflammatory drugs with first occurrence of heart failure and with relapsing heart failure: the Rotterdam Study.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with first hospitalization for congestive heart failure (CHF). It is likely, however, that NSAIDs precipitate a relapse but are less likely to induce a first occurrence of (incident) heart failure. METHODS: A total of 7277 participants in the Rotterdam Study were followed up from the interview date until the first of the following events: a diagnosis of incident heart failure, death, removal, or end of the follow-up period. Excluded from the study population were all participants with prevalent heart failure at baseline. Exposure to NSAIDs and other medication was calculated on the basis of automated data on filled drug prescriptions in the pharmacies within the study area. In a second analysis, we followed up all participants with incident heart failure until the first relapse or the end of follow-up. RESULTS: Incident heart failure was encountered in 345 participants during follow-up. Current use of NSAIDs was associated with a relative risk of incident heart failure of 1.1 (95% confidence interval [CI], 0.7-1.7), after adjustment for age, sex, and concomitant medication. In patients with prevalent heart failure who filled at least 1 NSAID prescription since diagnosis of heart failure, the univariate and adjusted relative risks of a relapse were 3.8 (95% CI, 1.1-12.7) and 9.9 (95% CI, 1.7-57.0), respectively. CONCLUSIONS: The use of NSAIDs is not associated with an increased risk of incident heart failure. In patients with prevalent heart failure, current use of NSAIDs is associated with a substantially increased risk of a relapse.

Aged↗
PubMed1996

Cold storage of the heart with University of Wisconsin solution and 2,3-butanedione monoxime: Langendorff vs isolated working rabbit heart model.

Currently, for clinical heart preservation with University of Wisconsin (UW) solution the ischemic time is limited to 8 h. The reliable preservation of the heart for 24 h or more would have a dramatic impact on the existing practice of cardiac transplantation. We showed previously [J. Thorac. Cardiovasc. Surg. 107; 764-775 (1994)] that experimentally preservation could be extended to 24-30 h by preventing ischemic contracture of the heart with 2, 3-butanedione monoxime (BDM) in the UW solution (UWBDM). This resulted in nearly 100% return of function as tested in the isolated crystalloid-reperfused rabbit heart in the nonworking Langendorff preparation. We have confirmed these results and now have measured the function of hearts stored in UWBDM for 2, 4, 12, and 24 h using the isolated working rabbit heart model. Preservation in UWBDM solution resulted in a biphasic decrease of cardiac output. In the hearts preserved for 2-12 h the decrease of function averaged 20-35% upon reperfusion, and the differences at 2, 4, or 12 h were not significant (analysis of variance p > 0.05). A more pronounced decrease of 64% was obtained after 24 h of cold storage. Hearts preserved for 24 h without BDM were practically nonfunctional. The release of enzymes (creatine kinase and lactate dehydrogenase) followed biphasic pattern similar to that of cardiac output: a small release between 2 and 12 h and larger, significant losses at 24 h. Although we originally proposed that hearts preserved with UWBDM for 24 h were well preserved (Langendorff model), we now show that poor function was obtained at 24 h. The difference was that in this study we used a more rigorous, isolated working rabbit heart model to test the function of the preserved heart, and this may be a better test of preservation quality.

Adenosine↗
PubMed2000

Heart and gut chiralities are controlled independently from initial heart position in the developing zebrafish.

A fundamental problem in developmental biology is how left-right (LR) asymmetry is generated, both on the whole organism level and at the level of an individual organ or structure. To investigate the relationship of organ sidedness to organ chirality, we examined 12 zebrafish mutants for initial heart tube position and later heart looping direction (chirality). Anomalous initial heart position was found in seven mutants, which also demonstrated loss of normal LR asymmetry in lateral plate mesoderm (LPM) antivin/lefty-1 and Pitx2 expression. Those with a relatively normal notochord (cyc(b16), din, and spt) displayed a predictive correlation between initial heart position and heart chirality, whereas initial heart position and heart chirality were independently randomized in those with a defective notochord (flh, boz, ntl, and mom). The predictability of heart chirality in spt, din, and b16 embryos, even in the absence of normal antivin/lefty-1 and Pitx2 expression, strongly suggests that heart chirality is controlled by a process distinct from that which controls appropriate left-sided LPM expression of antivin-Pitx2 signaling pathway molecules. In addition, there was correlation of initial heart position with gut chirality (and also between heart chirality and gut chirality) in the first class of mutants with normal notochord, but not in the second class, which appears to model human heterotaxy syndrome.

Animals↗
PubMed2003

Sheep heart RNA stimulates myofibril formation and beating in cardiac mutant axolotl hearts in organ culture.

In the Mexican axolotl, Ambystoma mexicanum, recessive mutant gene c, when homozygous, results in a failure of the heart to form sarcomeric myofibrils and contract normally. Previous studies have shown that purified RNA from normal anterior endoderm or from medium conditioned with anterior endoderm/pre-cardiac mesoderm has the capacity to rescue mutant hearts in organ culture. In the present study, RNA extracted from adult sheep heart was tested for its capacity to promote differentiation in the mutant axolotl hearts. Mutant hearts cultured in the presence of the sheep heart RNA in Steinberg's solution for 48 h displayed rhythmic contractions. Ultrastructural studies showed that the rescued mutant axolotl ventricular myocardial cells contained myofibrils of normal morphology. Mutant hearts cultured in Steinberg's solution alone did not beat throughout their lengths and myofibrils were not observable in the ventricles. Confocal microscopy confirmed the increase of Tropomyosin expression and formation of myofibrils in mutant hearts treated by sheep heart RNA. Thus, sheep heart RNA promotes myofibrillogenesis and the development of contractile function in embryonic cardiac mutant axolotl hearts.

Ambystoma mexicanum↗