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PubMed1995

Functional and ultrastructural alterations of canine myocardium subjected to very brief coronary occlusions.

The effects of very brief and recurrent coronary occlusions on myocardial regional shortening and its ultrastructure have been analysed. Ultrasonic crystals were implanted in the left ventricular subendocardium of 23 anaesthetized dogs with the thorax open, to measure the shortening fractions of an ischaemic and a control segment. Twenty 2 min total occlusions were provoked in the left anterior descending coronary artery, with 3 min recovery intervals (reperfusion) between occlusions. The shortening fraction decreased progressively with each occlusion, reaching a value 18.9% lower than the basal after the last ischaemic episode (P < 0.05); 32.3% after 4 h of reperfusion (P < 0.01), and 28.6% after 24 h (P < 0.01). Qualitative and quantitative ultrastructural analysis showed an increase in the mitochondrial volume of the ischaemic tissue (158% vs control, P < 0.001) with significant damage to the cell components (7.7-fold increases vs control mitochondria). These results show that when the myocardium is subjected to very brief and repeated coronary occlusions, there is progressive deterioration of systolic function with structural alterations, mainly at the mitochondrial level. These modifications are still observable 24 h after the end of ischaemic stimulation and could be the cause of transitory and/or chronic systolic dysfunctions in the absence of previous heart attack.

Animals↗
PubMed1981

Left ventricular diastolic pressure-volume relations in rats with healed myocardial infarction. Effects on systolic function.

To determine the effects of healed myocardial infarction on the diastolic compliance of the left ventricle, we studied 36 rats 26 days after left coronary artery ligation. Peak cardiac output and stroke volume were measured under ether anesthesia during volume loading, and peak left ventricular developed pressure was determined during occlusion of the ascending aorta. During a slow infusion of saline into the potassium-arrested left ventricle, diastolic pressure and volume were measured continuously over the pressure range -5 to 30 mm Hg. Infarct size was determined by planimetry of serial sections taken from each heart at 1-mm intervals from apex to base. In rats with healed infarcts, left ventricular volume was increased in proportion to infarct size and the diastolic pressure-volume relationship was shifted so that at pressures below 2.5 mm Hg volume was increased, resulting in an increased ventricular compliance in this low pressure range. Above this pressure, the slopes of the pressure-volume curves were similar in rats with and without infarctions. Peak cardiac output and pressure-generating capacity were impaired in proportion to infarct size. This impairment of cardiac performance correlated with the infarct size-related increase in diastolic volume, which served to offset the reduction in flow generating capacity caused by systolic dysfunction, while contributing directly to the impairment of pressure generating capacity.

Animals↗
PubMed1998

Dopamine and dobutamine have different effects on heart rate variability in patients with congestive heart failure.

BACKGROUND: Autonomic dysfunction plays an important role in the pathogenesis, treatment and prognosis of congestive heart failure (CHF). Sympathomimetic amines have been widely used in the treatment of CHF, but reports on their autonomic effects in CHF are rare. This study was designed to evaluate the effects of dopamine and dobutamine on cardiac autonomic function as assessed by heart rate variability (HRV). METHODS: Twenty patients with symptomatic CHF (systolic dysfunction) were enrolled. After recording one-hour baseline electrocardiographs (ECGs), patients were randomly selected for either dopamine (4 micrograms/kg/minute, Group A) or dobutamine (4 micrograms/kg/minute, Group B) treatment for three days. On the third day, a 24-hour ambulatory ECG was recorded and a tilt-table test was performed. Only furosemide and nitrates were allowed for adjunctive therapy. HRV was measured before and after treatment in both time and frequency domains. Frequency-domain HRV was also measured during head-up tilt. RESULTS: After treatment, all patients improved [New York Heart Association fraction (NYHA Fc) 3.7 to 2.0]. Group A patients had higher post-treatment 24-hour HRV than those in Group B. SDNN (standard deviation of the average normal RR intervals in the entire ECG recording), SDANN (standard deviation of the average normal RR intervals for all five minute segments of an entire ECG recording) and SDNN indices in Group A were significantly higher than in Group B (90 +/- 33 ms vs 41 +/- 12 ms, 78 +/- 32 ms vs 36 +/- 11 ms, and 37 +/- 19 ms vs 16 +/- 7 ms, respectively, all p < 0.05). rMSSD (the square root of the mean of the squared differences between adjacent normal RR intervals over the entire ECG recording) and pNN50 (percentage of differences between adjacent normal RR intervals that are greater than 50 ms computed over the entire ECG recording) were also higher in Group A patients, with borderline significance. All measurements of total frequency and low-frequency and high-frequency components tended to be higher in Group A than Group B, but this was only significant for total frequency amplitude (22.9 +/- 13.4 ms vs 10.9 +/- 6.1 ms, p < 0.05). Dopamine but not dobutamine treatment seems to restore the depressed circadian change in frequency-domain HRV classically seen in patients with CHF. The HRV change during head-up tilting did not differ between the two groups. Three patients in Group B showed non-sustained ventricular tachycardia on ambulatory ECG during the treatment period. CONCLUSIONS: Dopamine and dobutamine have comparable therapeutic effects in patients with CHF, but low-dose dopamine more favorably affects cardiac autonomic function.

Aged↗
PubMed2003

Enoximone echocardiography: a novel test to evaluate left ventricular contractile reserve in patients with heart failure on chronic beta-blocker therapy.

BACKGROUND: It has been suggested that an extensive contractile reserve identified recognised by means of dobutamine stress echocardiography may predict a better prognosis in patients with severe left ventricular dysfunction at rest. However, the clinical use of dobutamine stress echocardiography may be limited in patients with chronic heart failure by the substantial proportion of such patients treated with beta-blockers, since the inotropic response to adrenergic stimulation is known to be attenuated in patients receiving beta-adrenoceptor blockers. Enoximone is a positive inotropic agent that inhibits cyclic adenosine monophosphate-specific phosphosdiesterase. We therefore tested the hypothesis that enoximone may be an alternative to dobutamine in evaluating left ventricular contractile reserve in patients with systolic dysfunction on chronic beta-blocker therapy. METHODS: We studied 26 patients (21 males and five females) with a mean age of 58 PlusMinus; 10 years: 11 were not receiving beta-blockers (noBB group); 15 were receiving carvedilol at a mean dose of 34 mg/day (BB group). Dobutamine was infused at doses of 5 and 10 micrograms/kg/min, and enoximone at a dose of 1.5 mg/kg. RESULTS: The ejection fraction in the noBB group increased by 9% with dobutamine and 8.73% with enoximone (p = 0.86); in the BB group, it increased by 6% with dobutamine and 8.94% with enoximone (p = 0.03). Regional peak systolic velocities were evaluated by means of tissue Doppler imaging in four basal and four medium level segments. In the noBB group, they increased more with dobutamine than with enoximone in three of the eight segments; no significant differences were found in the BB group. Dobutamine induced non-sustained ventricular tachycardia in three patients and supraventricular tachycardia in one, whereas enoximone did not induce any repetitive arrhythmias. CONCLUSIONS: Enoximone might be preferable to low-dose dobutamine for evaluating left ventricular contractile reserve in chronically beta-blocked heart failure patients as it is slightly more potent and has a better safety profile.

Adrenergic beta-Antagonists↗
PubMed1987

Early postoperative changes in left ventricular chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: a prospective two-dimensional echocardiographic study.

We prospectively studied 16 patients with isolated aortic stenosis and eight with isolated aortic regurgitation undergoing aortic valve replacement, using two-dimensional echocardiography preoperatively, intraoperatively, and 41 +/- 7 days postoperatively to calculate the intraoperative change in afterload, quantify the postoperative changes in left ventricular chamber size, architecture, load and function, determine whether the postoperative left ventricular remodeling correlated with the intraoperative change in afterload in aortic stenosis and aortic regurgitation, and assess whether preoperative afterload excess precluded postoperative improvement in left ventricular function. Preoperative left ventricular mass, end-systolic meridional and circumferential wall stresses, ejection fraction, and stress-shortening relations in patients with aortic stenosis and aortic regurgitation were similar. However, our patients with aortic regurgitation had severe systolic dysfunction, with ejection fraction less than 55% in all but one patient, compared with only 10 of 16 patients with aortic stenosis. Left ventricular end-diastolic volume, mass/volume ratio, and chamber shape were significantly different in patients with aortic stenosis and aortic regurgitation (174 +/- 64 vs 294 +/- 140 ml, p less than .01; 1.81 +/- 0.63 vs 1.14 +/- 0.18, p less than .01; and 0.59 +/- 0.09 vs 0.69 +/- 0.09, p less than .05, respectively). Intraoperative end-systolic meridional and circumferential stresses fell significantly in patients with aortic stenosis but remained unchanged in those with aortic regurgitation. The changes in left ventricular volume and ejection fraction during early postoperative remodeling (6 weeks) correlated with the intraoperative change in afterload in patients with aortic stenosis. In contrast, there was no intraoperative change in afterload in patients with aortic regurgitation and no significant changes in left ventricular volume, architecture, or function at 6 weeks or at 6 months. The differences in left ventricular remodeling and changes in function between patients with aortic stenosis and aortic regurgitation in the early postoperative period most probably relates to the major difference in intraoperative reduction in afterload, although a contributory role may have been played by the preoperative left ventricular dysfunction in those with aortic regurgitation that was underestimated by measurement of ejection fraction.

Adult↗
PubMed1999

[Anesthetic management for pericardial fenestration in a hypertrophic cardiomyopathy (HCM) patient with massive pericardial effusion].

A 65 year-old male with HCM had progressively increased pericardial effusion. He also had atrial fibrillation (af), cardiac systolic dysfunction and chronic renal failure needing hemofiltration. Pericardial fenestration was carried out to improve diastolic function. Anesthetic management with fentanyl plus low-dose propofol infusion and postoperative analgesia with epidural morphine were effective for hemodynamic stability to prevent myocardial depression and to control ventricular response to atrial fibrillation. Intraoperative trans-esophageal echocardiography (TEE) monitoring was very useful for fluid therapy, inotropic support and estimation of systolic and diastolic function.

Aged↗
PubMed2006

The relationship between myocardial extracellular matrix remodeling and ventricular function.

Elevations in myocardial stress initiate structural remodeling of the heart in an attempt to normalize the imposed stress. This remodeling consists of cardiomyocyte hypertrophy and changes in the amount of collagen, collagen phenotype and collagen cross-linking. Since fibrillar collagen is a relatively stiff material, a decrease in collagen can result in a more compliant ventricle while an increase in collagen or collagen cross-linking results in a stiffer ventricle. If continued elevations in wall stress exceed the ability of the heart to compensate, then the ventricular wall thickness is disproportionately reduced compared to chamber volume and diastolic and systolic dysfunction ensues. This review describes the structural organization of collagen within the myocardium, discusses its effect on ventricular function and considers whether therapy aimed at reducing fibrosis is efficacious in heart failure. The evidence indicates that chamber stiffness can clearly be affected by alterations in both collagen quantity and quality, with the effect of changes in collagen concentration being modified by the extent of collagen cross-linking. The limited evidence available regarding the effects of collagen on systolic function indicates that pharmacological attempts to reduce interstitial collagen have a negative impact. Accordingly, a shift in treatment strategies directed more specifically at affecting collagen cross-linking, rather than reducing the concentration of collagen, may be warranted in the prevention of the adverse impact of collagen alterations on myocardial remodeling.

Cardiomegaly↗
PubMed1994

Altered sarcolemmal calcium channel density and Ca(2+)-pump ATPase activity in tachycardia heart failure.

Whether sarcolemmal (SL) calcium handling is altered in endstage heart failure produced by chronic rapid pacing is not known. To investigate this we paced 7 rabbits at a rate of 400 beats/min for 35 +/- 11 days. 6 animals served as non-paced controls. Purified left ventricular SL membranes were then prepared and tested for [3H]-nitrendipine binding and (Ca(2+) + Mg2+)-dependent ATPase (Ca(2+)-pump) activity. Results show a 50% reduction in calcium channel antagonist binding sites with Bmax values reduced from 450 +/- 40 to 230 +/- 8 fmoles/mg protein in response to chronic rapid pacing (P < 0.01). This change was accompanied by a modest decrease in Kd from 0.29 +/- 0.09 to 0.22 +/- 0.03 nM (not significant). Vmax values for the SL Ca(2+)-pump ATPase were decreased from 387 to 164 nmoles/mg protein/min (P < 0.01) with KCa2+ values reduced from 0.91 to 0.28 microM Ca2+ (P < 0.05) in response to tachycardia induced failure as compared to controls. ATPase activity in both groups was very sensitive to 25 microM calmidazolium and 5 microM vanadate. Results from this study indicate that both a reduction in SL calcium channel density and decrease in SL Ca(2+)-pump ATPase activity are evident in tachycardia heart failure. We conclude that sarcolemmal calcium handling is altered in heart failure induced by chronic rapid pacing and that such changes may contribute to systolic dysfunction associated with this model to heart failure.

Animals↗
PubMed1999

Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy.

BACKGROUND: Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process. MATERIALS AND METHODS: Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler. Left atrial volume (cm3/m2) at mitral valve opening (maximal, Vmax.), onset of atrial systole (P wave of the electrocardiogram, Vp), and mitral valve closure (minimal, Vmin. ) was determined with two-dimensional echocardiography using the biplane area-length method. The left atrial active emptying fraction (ACTEF = [Vp-Vmin.] x 100/Vp) served as an index of systolic function. RESULTS: The peak early diastolic transmitral flow velocity (cm/sec) was similar in the three groups (idiopathic: 60 +/- 16, ischemic: 58 +/- 20, control: 56 +/- 22; P = NS), whereas the late diastolic transmitral flow velocity was lower but not significantly different in idiopathic compared to ischemic cardiomyopathy, and in both was lower than control (26 +/- 12 vs. 34 +/- 13 vs. 44 +/- 14, respectively; P < 0.05). Vmax. and Vp were similar in idiopathic and ischemic cardiomyopathy and greater than control (44.6 +/- 13.6 vs. 48.2 +/- 18.3 vs. 26.9 +/- 6.2; P < 0.05, and 34.6 +/- 13.4 vs. 30.8 +/- 10.9 vs. 16.7 +/- 3.7, respectively; P < 0.05). ACTEF was lower in idiopathic than in ischemic cardiomyopathy and in the latter it was similar to control (18 +/- 10% vs. 32 +/- 10% vs. 36 +/- 10%, respectively; P < 0.05). Moreover, ACTEF was inversely related to left atrial tension at end-of atrial systole both in idiopathic and in ischemic cardiomyopathy (r2 = 0.52, P = 0.001 and r2 = 0.57, P = 0.0007, respectively). However, at any given level of left atrial tension at end of atrial systole, ACTEF was lower in idiopathic than ischemic cardiomyopathy. CONCLUSION: Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy despite similar left atrial loading conditions. This finding suggests left atrial myopathy in the former, and may be related to the differences in the response to medical treatment and clinical outcome observed between the two conditions.

Atrial Function, Left↗
PubMed2004

Predictors of haemodynamic instability and heart rate variability during haemodialysis.

BACKGROUND: The pathogenesis of haemodialysis-induced hypotension is multifactorial and may include autonomic nervous system dysfunction. The present study was undertaken to (i) determine heart rate variability (HRV) in chronic haemodialysis patients without and with haemodynamic instability (hypotension-prone) during ultrafiltration and (ii) identify patients at risk and the predictors of dialysis-related hypotension. METHODS: HRV was evaluated in 56 chronic haemodialysis patients without (stable; n = 27) and with symptomatic hypotension episodes (unstable; n = 29) during daytime, haemodialysis and night-time periods. Logistic regression analysis was performed in a model that included clinical and biochemical data and HRV measurements. RESULTS: HRV was significantly reduced in haemodynamically unstable as compared with the stable patients. LF/HF ratio, an index representative of sympathovagal balance, was significantly lower in unstable patients, especially in those with ischaemic heart disease and diabetes mellitus. In a logistic regression model including clinical data and HRV measurements, ischaemic heart disease and left ventricular systolic dysfunction were found to be the main predictors of haemodynamic instability. CONCLUSIONS: These data suggest that haemodynamic instability is strongly associated with a decreased HRV and an impaired sympathovagal balance, suggesting disturbed autonomic control in uraemic patients with cardiac damage. Patients with ischaemic heart disease, reduced left ventricular systolic function and decreased HRV may be at the highest risk to be haemodynamically unstable during haemodialysis. The role of early detection and treatment of ischaemic heart disease in preventing symptomatic hypotensive episodes in these patients remains to be determined.

Comorbidity↗
PubMed1999

Cardiac sympathetic denervation in familial amyloid polyneuropathy assessed by iodine-123 metaiodobenzylguanidine scintigraphy and heart rate variability.

Familial amyloid polyneuropathy (FAP) is a rare and severe hereditary form of amyloidosis, due to nervous deposits of a genetic variant transthyretin produced by the liver and characterized by both sensorimotor and autonomic neuropathy. Left ventricular systolic dysfunction is rare, but conduction disturbances and sudden deaths can occur. The neurological status of the heart has not been elucidated, and an alteration of the sympathetic nerves may be involved. We studied 17 patients (42+/-12 years) before liver transplantation by iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy, heart rate variability analysis, coronary angiography, radionuclide ventriculography, rest thallium single-photon emission tomography (SPET) and echocardiography. Coronary arteries, left ventricular systolic function and rest thallium SPET were normal in all patients. Only mild evidence of amyloid infiltration was found at echocardiographic examination. Cardiac MIBG uptake was dramatically decreased in patients compared with age-matched control subjects (heart-to-mediastinum activity ratio at 4 h: 1.36+/-0.26 versus 1.98+/-0.35, P<0.001), while there was no difference in MIBG washout rate. Heart rate variability analysis showed a considerable scatter of values, with high values in four patients despite cardiac sympathetic denervation as assessed by MIBG imaging. The clinical severity of the polyneuropathy correlated with MIBG uptake at 4 h but not with the heart rate variability indices. Cardiac MIBG uptake and the heart rate variability indices did not differ according to the presence or absence of conduction disturbances. Patients with FAP have sympathetic cardiac denervation as assessed by MIBG imaging despite a preserved left ventricular systolic function and cardiac perfusion, without correlation with conduction disturbances. Results of the heart rate variability analysis were more variable and this technique does not seem to be the best way to evaluate the extent of cardiac sympathetic denervation in FAP patients.

3-Iodobenzylguanidine↗
PubMed2005

Is there an association between ephedra and heart failure? a case series.

BACKGROUND: Ephedra is a sympathomimetic commonly used for the purposes of athletic performance enhancement and weight loss. It is known to be associated with gastrointestinal and psychiatric manifestations. We report here on 6 cases of dilated cardiomyopathy associated with ephedra use. METHODS AND RESULTS: Over a period of 18 months, 6 patients attending our outpatient department with new onset heart failure were noted to have exposure to ephedra. The case record was reviewed and detailed clinical and echocardiographic data were extracted. All 6 patients (4 males) had left ventricular dysfunction at presentation (mean ejection fraction 20 +/- 5%) and were treated with conventional heart failure pharmacotherapy. All patients discontinued ephedra use as advised. New York Heart Association class improved from class III in 5 patients (class II in 1 patient) to class I, within a median of 6 months (range 3-96). Ejection fraction improved to a mean of 47 +/- 6%. CONCLUSIONS: Ephedra may be associated with left ventricular systolic dysfunction. Withdrawal of this agent, in conjunction with proven pharmacotherapy, results in a significant improvement in functional status and left ventricular ejection fraction. We recommend specific enquiry into the use of over-the-counter supplements, particularly ephedra and its derivatives, when being evaluated with heart failure symptoms. These cases illustrate the potential risk of ephedra and provide additional support for the recent decision to ban this supplement.

Adult↗
PubMed2003

Left ventricular mass and systolic performance in pediatric patients with chronic renal failure.

BACKGROUND: Children with chronic renal disease have a high prevalence of left ventricular hypertrophy (LVH), which is thought to be adaptive to improve contractility and lower wall stress in the face of increased afterload and preload. The aim of this study was to determine the association between LV mass, LV performance, and LV contractility in children with chronic renal insufficiency (CRI) and children undergoing chronic dialysis. METHODS AND RESULTS: Twenty-five children with CRI, 12 undergoing chronic dialysis, and 24 controls had echocardiographic evaluation during rest and peak exercise. LV performance was assessed by calculation of shortening fraction and heart rate-corrected velocity of circumferential fiber shortening (VCF). Contractility (VCF difference) was determined based on the relation between VCF and end-systolic wall stress. Contractile reserve was assessed by the difference between contractility at rest and peak exercise. The dialysis group had higher LVM index than the group with CRI (42.9+/-10.3 versus 29.9+/-9.4 g/m(2.7), P<0.001). Both groups had higher LVM index compared with controls (22.2+/-6.1 g/m(2.7), P<0.001). At rest, the CRI and dialysis groups had significantly higher VCF(c) (P<0.001) and VCF difference (P<0.05) and significantly lower wall stress (P<0.01) compared with the control group. Dialysis patients had significantly lower contractile reserve compared with the control group (P<0.03). CONCLUSIONS: These results indicate that children with CRI and undergoing chronic dialysis have increased LVM, LV performance, and contractility at rest. However, dialysis patients have diminished contractile reserve during exercise, which might be an indicator for the development of more severe systolic dysfunction over time.

Adolescent↗
PubMed1993

Vasodilator therapy for congestive heart failure. Lessons from mortality trials.

Congestive heart failure is a major clinical and public health problem affecting between 2 and 3 million people in the United States. Whereas myocardial dysfunction assumes a central pathophysiologic role in the development of chronic heart failure, alterations in the peripheral vasculature and neurohormonal systems serve to modulate the heart failure state. Short-term studies of nonspecific vasodilators and angiotensin-converting enzyme inhibitors demonstrate a beneficial effect of these agents on left ventricular function, hemodynamics, exercise tolerance, and quality of life in patients with congestive heart failure and depressed left ventricular systolic function. More recently, several large-scale multicenter trials have documented improved survival in patients with heart failure who received vasodilating agents. These studies, in conjunction with hemodynamic and functional studies, argue strongly for the widespread use of vasodilator therapy, notably the angiotensin-converting enzyme inhibitors, for congestive heart failure and left ventricular systolic dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Graves' disease and low-output cardiac dysfunction: implications for autoimmune disease in endomyocardial biopsy tissue from eleven patients.

Classic high-output thyrotoxic heart disease is generally considered a direct effect of thyroid hormone. In contrast, the cause of the less common low-output heart failure is generally unknown. The aim of this study was to retrospectively evaluate available endomyocardial biopsy tissue from patients with coexistent Graves' disease and idiopathic low-output heart failure and determine whether the biopsy features were consistent with an autoimmune process. The study group consisted of 11 patients whose mean age was 47 years when they were diagnosed with hyperthyroidism and 52 years when diagnosed with cardiac dysfunction. Right ventricular endomyocardial biopsy tissue revealed severe lymphocytic myocarditis in a patient with severe ophthalmopathy and showed borderline myocarditis in a patient without ophthalmopathy. Biopsy tissues from 6 other patients showed appreciable myocyte hypertrophy and interstitial fibrosis, consistent with dilated cardiomyopathy. Two patients had nondiagnostic biopsy specimens, and 1 patient had features suggestive of arrhythmogenic right ventricular dysplasia. In conclusion, for the 11 patients with Graves' disease and unexplained systolic dysfunction, only 2 (18%) had lymphocytic infiltrates consistent with an autoimmune process. Thus, among patients with Graves' disease, most cases of low-output cardiac dysfunction appear to be due to causes other than an active autoimmune inflammatory process.

Autoimmune Diseases↗
PubMed1992

[Prognostic aspects in the treatment of chronic heart insufficiency].

Treatment of patients with heart failure due to major ventricular systolic dysfunction should aim not only at symptomatic but also at prognostic improvement. If correction of the underlying problem is not possible, treatment should slow down the progression of cardiac failure and eliminate triggers for sudden cardiac death due to electromechanical dissociation or arrhythmias. In every patient with chronic congestive heart failure screening for myocardial ischemia and complete revascularization is mandatory, if possible. In patients with coronary artery disease and diminished systolic function, beta-blockade may improve prognosis by reducing ischemic events and sudden cardiac death. The incidence of life-threatening arrhythmias in patients with heart failure may be reduced by eliminating facilitating factors like electrolyte disturbances, altered autonomic tone and raised intracardiac pressure rather than by antiarrhythmic medical treatment itself. One of the most important prognostic aspects in treatment is the interference with the development of the cardiomyopathy of overload, uniformly observed in chronic congestive heart failure. Modification of mechanical and neuroendocrine stimuli may postpone myocardial hypertrophy and interstitial hyperplasia as a consequence of altered gene expression. Early treatment with ACE inhibitors and in certain patients with betablockers are the most promising strategies to delay the progression of the disease. In contrast, positive inotropic drugs, including digitalis and phosphodiesterase inhibitors, do not improve prognosis. Calcium antagonists should also be used with restriction, as Verapamil and Diltiazem, but also Nifedipine may adversely affect the outcome in congestive heart failure patients.

Arrhythmias, Cardiac↗
PubMed1998

Long-term follow up of patients with endomyocardial fibrosis: effects of surgery.

AIMS: To determine the long-term outcome of patients with endomyocardial fibrosis and to compare echocardiographic and haemodynamic data before and after ventricular endocardial resection. PATIENTS: Seventeen patients (11 women and six men; mean age 35.5 years) diagnosed with endomyocardial fibrosis at the University Hospital in Zurich, Switzerland from 1971 to 1995. Twelve patients (70%) had partial obliteration of both ventricles and in five patients (30%) the fibrotic lesions were limited to the left ventricle. METHODS: Fourteen of the 17 patients had surgical resection: fibrosis was resected from both ventricles in five patients and from the left ventricle only in nine patients. Ten patients had mitral valve replacement and two had tricuspid valve replacement. Left ventricle endocardial resection was done without reconstruction or replacement of the atrioventricular valve in three patients. Preoperative and postoperative echocardiographic data were available for 11 patients and haemodynamic data for six patients. Patients were followed up for 0.4-19 years (mean 8.6). RESULTS: Preoperatively four patients were NYHA functional class IV and 10 were class III; postoperatively one patient was class III, seven class II, and six class I. Preoperatively, echocardiography showed obliteration of the left ventricular apex and inflow tract in all patients, which decreased or disappeared after surgery. Left ventricular end diastolic pressure decreased from 25 mm Hg before surgery to 14 mm Hg after successful resection of the fibrosis. Left ventricular and diastolic volume (normal 93 (17) ml/m2) increased from 65 ml/m2 to 97 ml/m2 (p < 0.05) after surgery. Ejection fraction was normal preoperatively (57%) and decreased slightly (52%) after surgery. One patient died five months after surgery from heart failure. Four surgically treated patients died during the follow up period: one each from systolic dysfunction, recurrence of endomyocardial fibrosis, pneumonia, and food poisoning. Overall survival was 65% at five years and 59% at 10 years; the survival rates of the operated patients was 72% and 68%, respectively. Only one of the medically treated patients survived longer than three years from diagnosis. CONCLUSIONS: Endomyocardial fibrosis is a rare disease in European countries and is found mainly in women. The clinical picture is characterised by severe congestive heart failure but heart size is only moderately increased. Systolic performance is normal or only slightly depressed despite severe restriction to filling, atrioventricular valve regurgitation or both. Partial obliteration of the right and/or left ventricle may be detected by echocardiography. Endocardial resection with atrioventricular valve replacement is the treatment of choice with appreciable postoperative improvement and 10 year survival of approximately 70%.

Adolescent↗
PubMed2002

Relation of aortic distensibility determined by magnetic resonance imaging in patients > or =60 years of age to systolic heart failure and exercise capacity.

Aortic stiffness increases with advancing age and is associated with the age-related decline in exercise capacity in healthy persons. Previous studies have suggested that aortic compliance is reduced in heart failure (HF). Older persons with systolic HF can have particularly severe exercise intolerance. However, the relation between increased aortic stiffness and exercise intolerance in elderly patients with systolic HF has not been examined. Therefore, aortic distensibility of the proximal ascending aorta (assessed by magnetic resonance imaging) and exercise tolerance (assessed by maximal exercise ergometry with expired gas analysis) was measured in 28 subjects (10 healthy subjects aged 20 to 30 years, 10 healthy subjects aged > or =60 years, and 8 subjects aged > or =60 years with systolic HF). Compared with healthy older subjects, patients with systolic HF had markedly decreased distensibility of the proximal aorta (0.5 +/- 0.4 vs 2.2 +/- 1.2 10(-3) mm Hg(-1), p <0.002), decreased peak exercise volume of oxygen consumption (VO2) (858 +/- 248 vs 1,436 +/- 344 ml/min, p <0.001), and increased aortic wall thickness (3.6 +/- 0.7 vs 2.9 +/- 0.4 mm, p <0.04). Aortic distensibility was significantly correlated with peak VO2 (r = 0.80, p <0.0001) and remained so even after being adjusted for age and left ventricular (LV) ejection fraction. These data suggest that decreased aortic distensibility may contribute to exercise intolerance in older patients with HF due to LV systolic dysfunction.

Adult↗