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PubMed2003

[Establishment of a nurse-led heart failure clinic. Design and baseline data from the first two years].

INTRODUCTION: Previous studies on the effect of heart failure clinics have shown a reduction in hospitalizations, reduced cost and improved quality of life. MATERIAL AND METHODS: We report on the establishment of a heart failure clinic and its impact on heart failure hospitalizations. Since September 1, 1999, a heart failure clinic has been operated at the Frederiksberg University Hospital. The clinic was designed with both a diagnostic and a therapeutic unit. The diagnostic unit offers open access to all patients with suspected heart failure, either through referral from general practitioners or from the medical departments of the hospital. In case of confirmed systolic heart failure, the patient is referred to the therapeutic unit. RESULTS: During the two years of operation, a total of 510 patients were registered in a newly established database (HJERTER+). Of these, 352 (69%) were found to have clinical evidence of heart failure, and 304 (86% of the heart failure patients) had left ventricular (LV) systolic dysfunction (ejection fraction < or = 0.45). Before referral, most patients with LV dysfunction had been treated with no or insufficient dose of ACE inhibitor (55%), and one third received beta-blockers (32%). During the two years of operation of the clinic, there was a 23% decline in heart failure related hospital admissions to the department of cardiology. DISCUSSION: Patients with systolic heart failure are not always optimally treated. The establishment of a heart failure clinic offering the combination of diagnosing and managing congestive heart failure appears to be effective both in terms of therapy optimization and with respect to a concomitant decline in hospitalization for heart failure.

Aged↗
PubMed2005

[Collagen synthesis and heart failure].

Little is known about collagen metabolism in heart failure, with or without left ventricular systolic dysfunction. We studied serum concentrations of the carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type-I synthesis, and of the carboxy-terminal telopeptide of collagen type I (ICTP), a marker of collagen type-I degradation, in 70 patients admitted for heart failure (35 with depressed left ventricular systolic function and 35 with preserved left ventricular systolic function) and in 30 control subjects. Patients with kidney failure, liver disease, metabolic bone disease, rheumatic disease, recent (within 3 months) major trauma or surgery, or serious wounds were excluded. The concentration of the collagen synthesis marker, PIP, was higher in heart failure patients than control subjects, at 140+/-56.38 mg/L vs 113.66+/-36.6 microg/L, respectively (P=.01). However, there was no difference in the concentration of the collagen degradation marker, ICTP, between heart failure patients and control subjects, at 2.89+/-2.37 mg/L vs 2.26+/-1.7 microg/l, respectively. In heart failure patients, left ventricular systolic function had nonsignificant effect on the PIP or ICTP concentration.

Aged↗
PubMed1996

Improvement of left ventricular diastolic dysfunction in hypertensive patients 1 month after ACE inhibition therapy: evaluation by ultrasonic automated boundary detection.

The purpose of this study was to detect any improvement in left ventricular diastolic dysfunction in hypertensive patients 1 month after cilazapril therapy. Twenty-three patients, 5 men and 18 women (mean age, 53.52 +/- 9.10 years), with mild or moderate hypertension (160 +/- 13/98 +/- 10 mm Hg), and free of other cardiac or systemic diseases, were studied using ultrasonic automated boundary detection (ABD) and pulsed Doppler echocardiography, before and 1 month after a daily dose of 2.5 mg of cilazapril. The following new ABD diastolic indices were determined: the time rate of area change in early diastole (dA/dt)E, that in late diastole (dA/dt)A, and their ratio (dA/dt)E/(dA/dt)A, while Doppler transmitral flow measurements of left ventricular diastolic filling were also simultaneously recorded. The ABD results showed left ventricular diastolic dysfunction (LVDD) in 9 of 23 patients (39%) compared with the ABD values of 12 normal volunteers. Neither method revealed any significant difference before and after treatment in the patient group as a whole. However, in the group of 9 patients with diastolic dysfunction, the ABD ratio (dA/dt)E/(dA/dt)A was significantly improved after cilazapril therapy (1.20 +/- 0.21 versus 1.41 +/- 0.17; P < 0.05). We concluded that a large percentage (39%) of patients with mild or moderate hypertension had reduced diastolic performance of the left ventricle at a stage of the disease when systolic dysfunction and/or hypertrophy were not evident. Significant improvement of diastolic dysfunction in hypertensive patients could be detected by the proposed ABD new diastolic indices 1 month after cilazapril therapy. In conclusion, automatic boundary detection should be a useful non-invasive modality for the early diagnosis of left ventricular diastolic dysfunction, as well as early recognition of its improvement.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Myocardial viability as a determinant of the ejection fraction response to carvedilol in patients with heart failure (CHRISTMAS trial): randomised controlled trial.

BACKGROUND: The improvement in left-ventricular ejection fraction (LVEF) in response to beta blockers is heterogeneous in patients with heart failure due to ischaemic heart disease, possibly indicating variations in the myocardial substrate underlying left-ventricular dysfunction. We investigated whether improvement in LVEF was associated with the volume of hibernating myocardium (viable myocardium with contractile failure). METHODS: We did a double-blind, randomised trial to compare placebo and carvedilol for 6 months in individuals with stable, chronic heart failure due to ischaemic left-ventricular systolic dysfunction. We enrolled 489 patients, of whom 387 were randomised. Patients were designated hibernators or non-hibernators according to the volume of hibernating myocardium. The primary endpoint was change in LVEF, measured by radionuclide ventriculography, in hibernators versus non-hibernators, on carvedilol compared with placebo. Analysis was by intention to treat. RESULTS: 82 patients dropped out of the study because of adverse events, withdrawal of consent, or failure to complete the investigation. Thus, 305 (79%) were analysed. LVEF was unchanged with placebo (mean change -0.4 [SE 0.9] and -0.4 [0.8] for non-hibernators and hibernators, respectively) but increased with carvedilol (2.5 [0.9] and 3.2 [0.8], respectively; p<0.0001 compared with baseline). Mean placebo-subtracted change in LVEF was 3.2% (95% CI 1.8-4.7; p=0.0001) overall, and 2.9% (0.7-5.1; p=0.011) and 3.6% (1.7-5.4; p=0.0002) in non-hibernators and hibernators, respectively. Effect of hibernator status on response of LVEF to carvedilol was not significant (0.7 [-2.2 to 3.5]; p=0.644). However, patients with more myocardium affected by hibernation or by hibernation and ischaemia had a greater increase in LVEF on carvedilol (p=0.0002 and p=0.009, respectively). INTERPRETATION: Some of the effect of carvedilol on LVEF might be mediated by improved function of hibernating or ischaemic myocardium, or both. Medical treatment might be an important adjunct or alternative to revascularisation for patients with hibernating myocardium.

Adrenergic beta-Antagonists↗
PubMed2001

[Serum copper levels in patients with chronic heart failure associated with systolic left ventricular dysfunction and its relation to the severity of cardiac failure].

UNLABELLED: The authors examined the serum copper concentrations in a group of 40 patients with chronic heart failure and significant systolic left ventricular dysfunction with an ejection fraction of less than 35%. In 21 patients the examination was made on admission to hospital on account of deterioration of cardiac insufficiency (group A), in 19 patients with stable chronic cardiac failure the examination was made at the out-patient department (group B). Assessment of serum copper concentrations was made by the method of absorption spectrophotometry under standard conditions. Assessment of the ejection fraction of the left ventricle and dimensions of the cardiac compartments was made by two-dimensional echocardiography. The heart rate was assessed from the electrocardiogram at rest. RESULTS: The authors found statistically significantly higher copper concentrations in patients of group A (19.78 +/- 1.67 mumol/l) as compared with group B (14.80 +/- 1.54 mumol/l, p < 0.001). The correlation between copper concentrations, the left ventricular ejection fraction, dimensions of the cardiac compartments and heart rate are not significant. CONCLUSION: Serum copper concentrations in patients with chronic heart failure and significant systolic left ventricular dysfunction are related to the severity of the disease and are higher in patients admitted on account of cardiac insufficiency than in patients with stable cardiac failure.

Aged↗
PubMed1995

Right ventricular dysfunction in low output syndrome after cardiac operations: assessment by transesophageal echocardiography.

BACKGROUND: Low output syndrome after cardiac operations is associated with high morbidity and mortality rates. The contribution of right ventricular dysfunction to this syndrome has not been fully characterized. The purpose of this study was to evaluate the utility of transesophageal echocardiography to identify the frequency and the in-hospital mortality from right ventricular dysfunction in patients with this syndrome. METHODS: Seventy-five consecutive patients undergoing transesophageal echocardiography for low output syndrome early after cardiac operations were evaluated. The findings from transesophageal echocardiography were correlated with the type of surgical procedure, cross-clamp time, right heart hemodynamics, and coronary angiography. RESULTS: Right ventricular systolic dysfunction occurred in 36 patients (42%); in 17 patients it was isolated and in 19 patients it occurred in combination with left ventricular dysfunction. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or with prolonged ischemic time during cardiopulmonary bypass. Hemodynamic data were not useful to distinguish the group with postoperative right ventricular dysfunction. Patients with right ventricular dysfunction had a high (44%) in-hospital mortality rate. CONCLUSIONS: Right ventricular dysfunction occurs frequently in patients with low output syndrome after cardiac operations and is associated with a high in-hospital mortality rate. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication.

Adult↗
PubMed2006

Integrin activation in the heart: a link between electrical and contractile dysfunction?

Integrins mechanically link the cytoskeleton to the extracellular matrix in cardiac myocytes and are thereby involved in mechanotransduction. Integrins appear to be necessary for cardiac myocyte hypertrophy. To determine the effect of increased integrin ligation and signaling on adult cardiac function, a heart-specific truncated alpha(5) integrin (gain of function) was conditionally expressed in mice. Four days later, we observed an 80% reduction in amplitude of the QRS complex, profound systolic dysfunction, decreased connexin43, loss of gap junctions, and abnormal intercalated discs. Surprisingly, isolated left ventricular myocytes contracted normally and exhibited normal Ca(2+) transients. This suggested that cell/cell electrical and/or mechanical coupling was disrupted. To distinguish electrical from mechanical coupling deficits, we compared the papillary muscle force generated by electrically stimulated versus rapid cooling contractions in which intracellular Ca(2+) is released without electrical depolarization. Both were decreased in the transgenic muscle. However, electrically stimulated contractions were more significantly reduced than rapid cooling contractures. This suggests a component of cell/cell electrical uncoupling. Optical mapping revealed a loss of the normal elliptical isochronal activation pattern implying a loss of preferential conduction through gap junctions. For the first time, we have shown that integrins can regulate both mechanical and electrical coupling in the adult heart, even in the absence of primary hemodynamic alterations. Furthermore, we demonstrated that unregulated integrin activation leads to both contractile dysfunction and arrhythmias.

Animals↗
PubMed2004

Cardiac-specific disruption of the c-raf-1 gene induces cardiac dysfunction and apoptosis.

The Raf/MEK/extracellular signal-regulated kinase (ERK) signaling pathway regulates diverse cellular processes such as proliferation, differentiation, and apoptosis and is implicated as an important contributor to the pathogenesis of cardiac hypertrophy and heart failure. To examine the in vivo role of Raf-1 in the heart, we generated cardiac muscle-specific Raf-1-knockout (Raf CKO) mice with Cre-loxP-mediated recombination. The mice demonstrated left ventricular systolic dysfunction and heart dilatation without cardiac hypertrophy or lethality. The Raf CKO mice showed a significant increase in the number of apoptotic cardiomyocytes. The expression level and activation of MEK1/2 or ERK showed no difference, but the kinase activity of apoptosis signal-regulating kinase 1 (ASK1), JNK, or p38 increased significantly compared with that in controls. The ablation of ASK1 rescued heart dysfunction and dilatation as well as cardiac fibrosis. These results indicate that Raf-1 promotes cardiomyocyte survival through a MEK/ERK-independent mechanism.

Animals↗
PubMed2005

Managing the post-myocardial infarction patient with asymptomatic left ventricular dysfunction.

The percentage of post-myocardial infarction (MI) patients with asymptomatic left ventricular dysfunction (ALVD) is now estimated at 10%, and that number is expected to grow as reperfusion procedures increasingly become routine. Since average all-cause mortality risk in these patients is high (up to 27%), definitive diagnostics are recommended to screen all post-MI patients for ALVD, defined as left ventricular systolic dysfunction in the absence of heart failure symptoms. Post-MI management strategies for patients with ALVD target the two routes of progression to heart failure: (1) cardiac remodeling mediated by neurohormonal activation, and (2) continued and recurrent myocardial ischemic events. Clinical trials of neurohormonal antagonists in post-MI ALVD patients have shown that angiotensin-converting enzyme inhibitors attenuate left ventircular remodeling and that beta-blocker therapy reverses remodeling for patients already on angiotensin-converting enzyme inhibitor therapy. Neurohormonal antagonist therapy is also associated with significant reductions in sudden death in post-MI ALVD patients.

Adrenergic beta-Antagonists↗
PubMed2006

Peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a disorder in which initial left ventricular systolic dysfunction and symptoms of heart failure occur between the late stages of pregnancy and the early postpartum period. It is common in some countries and rare in others. The causes and pathogenesis are poorly understood. Molecular markers of an inflammatory process are found in most patients. Clinical presentation includes usual signs and symptoms of heart failure, and unusual presentations relating to thromboembolism. Clinicians should consider PPCM in any peripartum patient with unexplained disease. Conventional heart failure treatment includes use of diuretics, beta blockers, and angiotensin-converting enzyme inhibitors. Effective treatment reduces mortality rates and increases the number of women who fully recover left ventricular systolic function. Outcomes for subsequent pregnancy after PPCM are better in women who have first fully recovered heart function. Areas for future research include immune system dysfunction, the role of viruses, non-conventional treatments such as immunosuppression, immunoadsorption, apheresis, antiviral treatment, suppression of proinflammatory cytokines, and strategies for control and prevention.

Adolescent↗
PubMed1998

Diastolic dysfunction and altered energetics in the alphaMHC403/+ mouse model of familial hypertrophic cardiomyopathy.

An arginine to glutamine missense mutation at position 403 of the beta-cardiac myosin heavy chain causes familial hypertrophic cardiomyopathy. Here we study mice which have this same missense mutation (alphaMHC403/+) using an isolated, isovolumic heart preparation where cardiac performance is measured simultaneously with cardiac energetics using 31P nuclear magnetic resonance spectroscopy. We observed three major alterations in the physiology and bioenergetics of the alphaMHC403/+ mouse hearts. First, while there was no evidence of systolic dysfunction, diastolic function was impaired during inotropic stimulation. Diastolic dysfunction was manifest as both a decreased rate of left ventricular relaxation and an increase in end-diastolic pressure. Second, under baseline conditions alphaMHC403/+ hearts had lower phosphocreatine and increased inorganic phosphate contents resulting in a decrease in the calculated value for the free energy released from ATP hydrolysis. Third, hearts from alphaMHC403/+ hearts that were studied unpaced responded to increased perfusate calcium by decreasing heart rate approximately twice as much as wild types. We conclude that hearts from alphaMHC403/+ mice demonstrate work load-dependent diastolic dysfunction resembling the human form of familial hypertrophic cardiomyopathy. Changes in high-energy phosphate content suggest that an energy-requiring process may contribute to the observed diastolic dysfunction.

Adenosine Triphosphate↗
PubMed2004

Diabetic cardiomyopathy: recent evidence from mouse models of type 1 and type 2 diabetes.

Diabetic cardiomyopathy is defined as ventricular dysfunction of the diabetic heart in the absence of coronary artery disease. With the use of both in vivo and ex vivo techniques to assess cardiac phenotype, reduced contractile performance can be observed in experiments with mouse models of both type 1 (insulin-deficient) and type 2 (insulin-resistant) diabetes. Both systolic dysfunction (reduced left ventricular pressures and decreased cardiac output) and diastolic dysfunction (impaired relaxation) is observed in diabetic hearts, along with enhanced susceptibility to ischemic injury. Metabolism is also altered in diabetic mouse hearts: glucose utilization is reduced and fatty acid utilization is increased. The use of genetically engineered mice has provided a powerful experimental approach to test mechanisms that may be responsible for the deleterious effects of diabetes on cardiac function.

Animals↗
PubMed2000

Transesophageal echocardiography assessment of left atrial appendage function in untreated systemic hypertensive patients in sinus rhythm.

To assess left atrial appendage (LAA) function in hypertensive patients without treatment, transesophageal echocardiography (TEE) was performed in 46 hypertensive patients in sinus rhythm, aged 40 to 55 years, and in 16 control subjects (group I) without cardiovascular disease, aged 41 to 54 years. The hypertensive patients were divided into 2 groups according to left ventricular (LV) systolic function: group II, the group with normal LV systolic function (ejection fraction 0.63 +/- 0.08), and group III, the group with LV systolic dysfunction (ejection fraction 0.39 +/- 0.05). The LAA late emptying velocities (EVs) were significantly reduced in the hypertensive subgroups compared with the control group (P <.001), but no significant difference in the LAAEV was found between groups II and III. The LAAEV in the hypertensive patients had a significant negative correlation with diastolic blood pressure, systolic blood pressure, and left atrial (LA) diameter. The maximal LAA areas were significantly larger in the hypertensive subgroups than in the control group (P <.05). No significant difference in LAA maximal area existed between groups II and III. The maximal LAA area in the hypertensive patients had a significant positive correlation with diastolic blood pressure, systolic blood pressure, and LA diameter, but a significant negative correlation with LV ejection fraction. With TEE, LA spontaneous echocardiographic contrast (SEC) was present in 6 (43%) of 14 patients in group III (P <.01) and in 7 (22%) of 32 patients in group II (P <.05). No significant difference in the occurrence of LASEC was found between groups II and III. Left atrial appendage thrombi by TEE were observed in 4 (29%) of 14 patients in group III (P <.05) and in 4 (13%) of 32 patients in group II (P = not significant). No significant difference in the occurrence of LAA thrombus existed between groups II and III. In conclusion, in patients with untreated hypertension, marked elevation of afterload imposed on the left atrium may involve both the left atrium and the LAA, resulting in impairment of LAA function. This condition may worsen with subsequent occurrence of SEC and later, thrombus formation. Therefore assessment of LAA function may be important even in the hypertensive patient in sinus rhythm.

Adult↗
PubMed2004

[Subclinical thyroid disease: subclinical hypothyroidism and hyperthyroidism].

Subclinical hypothyroidism (SHT) and subclinical hyperthyroidism (SCH) are defined as normal serum free T4 and T3 levels associated with elevated (SHT) or subnormal (SCH) serum TSH levels, respectively. Symptoms and signs of thyroid dysfunction are scarce. The prevalence is low. In SHT, total cholesterol and LDL-C are modestly elevated and levothyroxine may influence the lipids levels. There is decreased cardiac contractility and increased peripheral vascular resistance that improve with treatment. SCH is associated with atrial fibrillation, increased cardiac contractility and left ventricular mass, diastolic and systolic dysfunction that can be reversed with beta-adrenergic antagonists. Bone density is reduced in SCH. Depression, panic disorders and alterations in cognitive testing are frequent in SHT. Treatment of SHT is recommended for serum TSH levels greater than 8 mU/L and presence of thyroid antibodies. Endogenous SCH should be treated for serum TSH levels less than 0.1 mU/L, in the presence of symptoms and in elderly patents.

Humans↗
PubMed1998

Left Ventricular Diastolic Function in a Population Sample of Elderly Men.

BACKGROUND AND METHODS: Echocardiography with Doppler has been widely used to assess left ventricular (LV) diastolic function. Interpretation of the diastolic indices that are derived, however, is confounded by the effects of physiological aging on the LV diastolic function. In this study, the usefulness of different Doppler-derived indices of LV diastolic function was assessed in elderly subjects by using data from a health screening survey of 584 men aged 70 years. RESULTS: The index of early versus late transmitral blood flow, the E/A ratio, was found to be reduced in the apparently healthy subgroup (n = 195) of the population (0.96 +/- 0.25) compared with previous data from middle-aged subjects. However, E/A ratios similar to those in the apparently healthy subjects were found in subjects with coronary heart disease (CHD), hypertension, and diabetes mellitus. Only subjects with systolic dysfunction (ejection fraction < 40%) showed a significantly decreased E/A ratio (0.79 +/- 0.21, P < 0.05) compared with the apparently healthy subjects. Isovolumic relaxation time (IVRT) was, however, significantly prolonged in subjects with CHD or hypertension compared with the apparently healthy subjects (139 +/- 32, 127 +/- 25, and 118 +/- 21 milliseconds, respectively; P < 0.01), whereas the E wave deceleration times (DT) were alike in both apparently healthy and unhealthy subjects. The diastolic and systolic components of the pulmonary venous blood flow were alike in apparently healthy and unhealthy subjects. Left atrial size was increased in all patients with disease, possibly indicating increased preload. CONCLUSION: In this population sample of elderly men, the commonly used E/A ratio did not distinguish between apparently healthy subjects and those with cardiovascular diseases such as CHD or hypertension, which are known to be associated with LV diastolic dysfunction in the middle-aged population. IVRT appeared to be the most sensitive of the Doppler-derived indices of LV diastolic function used in the present study, but for this variable, the differences between apparently healthy subjects and unhealthy subjects were small. Thus, the age-associated changes in LV compliance appear to override the impact of these disorders on indices of LV diastolic function in elderly populations.

Journal Article↗
PubMed2000

Are beta-blockers effective in patients who develop heart failure soon after myocardial infarction? A meta-regression analysis of randomised trials.

BACKGROUND: The great majority of post-infarction studies of beta-blockers were conducted in an era when these agents were widely held to be contra-indicated for the management of heart failure. We now know that beta-blockers are highly effective for the management of patients with chronic stable heart failure. However, there remains uncertainty about their role in the setting of post-infarction heart failure and ventricular dysfunction. AIM: the primary objective in this paper, was to investigate the extent to which heart failure or evidence of major cardiac dysfunction influenced outcome in previous trials of beta-blockers in heart failure after myocardial infarction. METHODS: We assessed the extent to which the inclusion of patients with heart failure or major cardiac dysfunction influenced outcome in randomised trials of long-term use of beta-blockade after myocardial infarction. The primary analysis was to assess the extent to which the proportion of patients included in each trial with heart failure influenced the relative odds of all-cause mortality in the trials. All randomised trials without crossover with treatment lasting more than one month and with 50 or more patients were considered. All those that provided information on the proportion of patients with heart failure or major cardiac dysfunction in the original or subsequent articles were included in the analysis. RESULTS: Overall treatment with a beta-blocker was associated with a 22.6% reduction in the odds of death (95% C1 11-32.3%). There were very few data on the effects of beta-blockers after myocardial infarction in patients with documented left ventricular systolic dysfunction. In the analysis that included heart failure as a factor, treatment with a beta-blocker was associated with a non-significant interaction with the presence of heart failure. However, because the group including heart failure patients were at higher risk, the absolute benefit of treatment with beta-blockers appeared greater in this group. CONCLUSIONS: This analysis suggests that the relative benefit of beta-blockers on mortality after a myocardial infarction is similar in the presence or absence of heart failure but that the absolute benefit may be greater in the former. However, as current clinical practice has changed radically from the time when the majority of these trials were conducted, further trial evidence would be desirable.

Adrenergic beta-Antagonists↗
PubMed1998

Trandolapril. An update of its pharmacology and therapeutic use in cardiovascular disorders.

UNLABELLED: Trandolapril is an orally administered angiotensin converting enzyme (ACE) inhibitor that has been used in the treatment of patients with hypertension and congestive heart failure (CHF), and after myocardial infarction (MI). Trandolapril is a nonsulfhydryl prodrug that is hydrolysed to the active diacid trandolaprilat. Trandolapril 2 mg once daily provides effective control of blood pressure (BP) over 24 hours in patients with mild to moderate hypertension, with a trough/peak ratio of BP reduction (as determined by 24-hour ambulatory monitoring) consistently > or = 50%. Trandolapril has similar antihypertensive efficacy to enalapril as indicated by several clinical trials. Combined therapy with trandolapril and sustained-release verapamil has a significantly greater antihypertensive effect than either agent alone. Only limited data are available on the use of trandolapril in patients with CHF, although ACE inhibitors as a class are recommended as first line therapy in such patients. In the Trandolapril Cardiac Evaluation (TRACE) study, trandolapril 1 to 4 mg once daily resulted in an early and long term reduction in all-cause mortality, including cardiovascular mortality, in patients with left ventricular (LV) dysfunction after an MI. Trandolapril therapy was commenced a mean 4.5 days after acute MI and continued for 24 to 50 months. At study end, the relative risk of death from any cause with trandolapril versus placebo was 0.78 (p = 0.001). The tolerability profile of trandolapril is similar to that of other ACE inhibitors. Most adverse events are mild and transient in nature, and include cough, asthenia, dizziness, headache and nausea. Trandolapril has no adverse effect on lipid or carbohydrate metabolism. CONCLUSIONS: trandolapril has a favourable pharmacological profile and an antihypertensive efficacy at least comparable to that of other ACE inhibitors. The pharmacological characteristics of trandolapril allow it to provide good 24-hour control of BP with once-daily administration. Trandolapril has also demonstrated some efficacy in a small number of patients with CHF. In addition, trandolapril provides long term protection against all-cause mortality in patients with LV dysfunction after MI. The results of the Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) study will determine its potential as a cardioprotective agent in patients with coronary artery disease and preserved LV function. Thus, trandolapril represents an effective, well-tolerated and convenient treatment option for patients with mild to moderate hypertension or LV systolic dysfunction after MI.

Aged↗
PubMedDate not supplied

[Effects of carbon dioxide baths and exercise on physical performance of patients with left ventricular dysfunction after myocardial infarction].

Carbon dioxide baths (CDB) and exercise have a good effect on clinical indices of the postinfarction period in patients suffering from postinfarction cardiosclerosis with impaired left ventricular function, especially in combined use. Patients on general CDB and/or exercise exhibited a significant increase in time of exercise and power of the threshold load, less frequent occurrence of ischemic depression of ST segment and dyspnea in performing bicycle exercise. CDB and exercise are especially beneficial for patients with systolic dysfunction.

Baths↗