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PubMed1999

[Alteration of the longitudinal function of the left ventricle in hypertensives with systolic function of normal appearance].

UNLABELLED: Left ventricular (LV) transverse function is often used by the echocardiography to evaluate the systolic function in arterial hypertension (HTN). It would be interesting to know whether the LV long axis systolic dysfunction may precede the abnormalities of the transverse function in hypertension (HTN). For that purpose we evaluated by echo 36 patients (24 males, 12 females) with LV concentric hypertrophic (Lvmi > 134 g/m2 for men and > 110 g/m2 for women). All subjects were free of coronary heart disease and heart failure. According to the dimensions of the LV wall chickness (WTh) the HTN were subdivided in two groups: Group 1: Wth (12-14 mm) and Group 2: WTh (> 14 mm). The patients were compared to 30 healthy persons (control group) matched for age and LV systolic function (Fractional Shortening). METHODS: LV long axis shortening was measured at the septal and lateral sides of the mitral annulus using M-mode from the apical four chamber view. RESULTS: Compared to control group, septal long axis shortening fell significantly (p < 0.05) in proportion to the degree of the wall thickness: control group: 21 +/- 2 mm. Group 1: 16 +/- 1 mm and Group 2: 14 +/- 1 mm. Lateral shortening was reduced only in the Group 2 (15 +/- 2 vs 20 +/- 2 mm) (p < 0.05). LV wall thickness correlated significantly (p < 0.05) to septal and lateral shortening respectively (r = -0.51) and (r = -0.48). CONCLUSIONS: 1. Significant impairment of LV long axis function occurs in arterial hypertension with concentric hypertrophy even with normal transverse systolic function. 2. This alteration seems to be related to the dimensions of the LV wall thickness. 3. The prognostic implication of this disorder should be investigated further.

Adult↗
PubMed1989

Significance of the transmural diminution in regional hydrogen ion production after repeated coronary artery occlusions.

Previous studies have revealed that the regional accumulation of ischemic metabolites including hydrogen ion (H+) and PCO2 diminish after repeated occlusions. We postulated that this diminution reflects a blunted metabolic response that is related to the severity of ischemic injury and, hence, may be most pronounced in subendocardial (ENDO) regions. To investigate this hypothesis, the left anterior descending coronary artery was serially occluded three times in 51 dogs for a period of either 3 minutes (n = 15), 5 minutes (n = 18), or 15 minutes (n = 18). Each occlusion was separated by 45 minutes of reperfusion. Myocardial [H+] was measured in the endomyocardium and in the epimyocardium of the ischemic anterior wall by use of miniature pH glass electrodes. Accumulation of H+ during occlusion (delta [H+]) in the ENDO region was significantly less during the second occlusion when compared with the first occlusion (3-minute occlusions: 28.2 +/- 3.7 nM/l vs. 39.4 +/- 5.4 nM/l, p less than 0.002; 5-minute occlusions: 49.8 +/- 5.0 nM/l vs. 72.1 +/- 6.5 nM/l, p less than 0.0002; 15-minute occlusions: 132.3 +/- 14.6 nM/l vs. 225.6 +/- 27.7 nM/l, p less than 0.0003). A similar trend was noted for delta [H+] in the subepicardial (EPI) regions. During occlusion, the rise in [H+] occurred sooner, and delta [H+] was consistently greater in the ENDO when compared with the EPI regions (p less than 0.05). Regional myocardial blood flow did not change during the three occlusions, indicating that the diminution in H+ accumulation stemmed from a decrease in H+ production and not from an increase in collateral flow. The decrement in H+ accumulation between the first and second occlusions (delta [H+]1-delta [H+]2) 1) was greater in the ENDO than in the EPI regions (p less than 0.05); 2) correlated with the duration of occlusion (ENDO: r = 0.66, p less than 0.001; EPI: r = 0.82, p less than 0.0001); and 3) was related to the impairment of anterior wall systolic shortening after the first reperfusion period. These findings suggest that the diminution in H+ production that follows serial coronary occlusions reflects a blunted metabolic response that is related to both the duration of ischemia and the degree of systolic dysfunction. Moreover, though attenuation of ischemic metabolite production occurs transmurally, it is most pronounced in the deep ENDO regions.

Animals↗
PubMed2002

Evidence of exercise-induced cardiac dysfunction and elevated cTnT in separate cohorts competing in an ultra-endurance mountain marathon race.

Cardiac damage has recently been implicated in the aetiology of "exercise induced cardiac dysfunction". The humoral markers of cardiac damage that have been utilised to date are not sufficiently cardio-specific to investigate this hypothesis. The aim of the present study was to examine cardiac function following prolonged exercise, and investigate the contention of cardiac damage utilising a new highly cardio-specific marker. Thirty-seven competitors in the 2-day Lowe Alpine Mountain Marathon 2000 volunteered for the study. Competitors were sub-divided into 2 groups. Group 1 (n = 11) were examined using echocardiography pre and post the event, examining left ventricular diastolic and systolic function. Group 2 (n = 26) had venous blood samples drawn prior to the event and immediately following day-1 and day-2. Blood samples were analysed for total creatine kinase activity (CK), creatine kinase isoenzyme MB(mass) (CK-MB(mass)), and cardiac troponin T. Echocardiographic results indicated left ventricular diastolic and systolic dysfunction following cessation of exercise. CK and CK-MB(mass) were both elevated following day-1, and immediately following race completion. Cardiac troponin T levels were below the 99th percentile (0.01 microg/L) in all subjects prior to the event, following day-1 cTnT was elevated above 0.01 microg/L in 13 subjects, but returned to below 0.01 microg/L following race completion on day-2. However, no individual data reached clinical cut-off levels for acute myocardial infarction (AMI) (0.1 microg/L). Two days arduous exercise over mountainous terrain resulted in cardiac dysfunction, and significant skeletal muscular degradation. The elevation of cTnT above the 99th percentile in the present study is suggestive of minimal myocardial damage. The clinical significance of and exact mechanism responsible for such damage remains to be elucidated.

Adult↗
PubMed2004

Aldosterone antagonism and congestive heart failure: a new look at an old therapy.

PURPOSE OF REVIEW: More than 5 million people in the United States alone have congestive heart failure, and an estimated 40 million have established risks and warrant therapy. Mineralocorticoid antagonists have emerged as a new paradigm for the treatment of congestive heart failure. They have established benefits among patients with chronic symptomatic systolic dysfunction, and recent studies have demonstrated substantial effect on the morbidity and mortality among patients with heart failure after myocardial infarction. The exact biologic mechanism is thus far unknown. RECENT FINDINGS: Within the last 5 years, efforts have intensified to help define better the biologic mechanisms by which mineralocorticoid receptor antagonisms exert the observed clinical benefit. Elegant human studies have demonstrated some important observations. First, under conditions of increased plasma aldosterone concentrations, the heart will extract aldosterone. Second, aldosterone extraction in the heart stimulates increased collagen turnover culminating in ventricular remodeling. Third, among people with chronic systolic or diastolic heart failure, aldosterone is actually produced and secreted by the heart. Finally, antagonism of the mineralocorticoid receptor will attenuate or abrogate many of these deleterious effects. SUMMARY: Combined clinical and detailed mechanistic investigations have established mineralocorticoid receptor antagonism as the new treatment paradigm for congestive heart failure. Recent clinical data have demonstrated that treatment of patients with a combination of mineralocorticoid receptor antagonism (eplerenone) and angiotensin converting enzyme-inhibitor (ACE-I) results in substantial reduction in left ventricular mass. Furthermore, a federally funded initiative to treat more than 6000 patients with diastolic heart failure with spironolactone is in its final phases of planning. It is foreseeable that, along with ACE-I and beta-blockers, mineralocorticoid receptor antagonism will become part of the treatment paradigm for people across the entire spectrum of cardiovascular disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Neurohormonal effects of furosemide withdrawal in elderly heart failure patients with normal systolic function.

BACKGROUND: In heart failure patients, diuretics cause renin-angiotensin-aldosterone system (RAS) activation, which may lead to increased morbidity and mortality despite short-term symptomatic improvement. AIM: To determine changes in RAS activation and clinical correlates following furosemide withdrawal in elderly heart failure patients without left ventricular systolic dysfunction. METHODS AND RESULTS: We performed clinical assessments and laboratory determinations of aldosterone, plasma renin activity (PRA), atrial natriuretic peptide (ANP), norepinephrine, and endothelin in 29 heart failure patients [aged 75.1+/-0.7 (mean+/-S.E.M.) years], before, 1 and 3 months after placebo-controlled furosemide withdrawal. Recurrent congestion occurred in 2 of 19 patients withdrawn, and in 1 of 10 patients continuing on furosemide. Three months after withdrawal, PRA had decreased -1.61+/-0.71 nmol/l/h (P<0.05). Decreases in aldosterone levels did not reach significance (-0.17+/-0.38 nmol/l). The decreases in PRA after withdrawal correlated with decreases in systolic (r(s)=0.61, P=0.020) and diastolic blood pressure (r(s)=0.80, P=0.01). Successful withdrawal was associated with increases in norepinephrine (+0.58+/-0.22 nmol/l) and ANP (+3.5+/-1.3 pmol/l) (P<0.05) after 1 month, but these changes did not persist after 3 months. Endothelin levels did not change in both groups. CONCLUSION: Successful furosemide withdrawal in elderly heart failure patients causes persistent decreases in RAS activation.

Aged↗
PubMedDate not supplied

Cardiac resynchronization therapy decreases the mitral coaptation point displacement in heart failure patients.

BACKGROUND: In patients with left ventricular (LV) dysfunction the mitral leaflet coaptation point (CPMA) is displaced towards the LV apex. The aim of our study was to estimate the value of CPMA measurement as a simple index regarding the acute effects of cardiac resynchronization therapy (CRT), which is coming to be an established method of treatment for congestive heart failure (CHF). METHODS: We studied 20 patients with CHF (NYHA III-IV) and LV ejection fraction (LVEF) 22 +/- 4%. All patients received CRT and an echocardiogram was performed within 24-48 hours. The echocardiographic indices LV end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD), LVEF, mitral annulus diameter (MAD), and the degree of intraventricular desynchronization, were measured at CRT off and CRT on. The CPMA, the distance between the coaptation point of the mitral leaflets and the mitral annulus, was measured from the apical 4-chamber view in end-systole at both CRT on and CRT off. RESULTS: CRT improved both the contractility and dimensional indices in CHF patients. CPMA decreased from 11.3 +/- 2 mm at CRT off to 9.1 +/- 1.8 mm after CRT on (p < 0.001) and MAD from 38.9 +/- 3.9 mm at CRT off to 37.5 +/- 3.7 mm at CRT on (p < 0.002). LVEF improved from 24.5 +/- 5.7% at CRT off to 29.5 +/- 5.1% at CRT on (p < 0.001). There was an improvement in LV synchronization from 88 +/- 7 ms at CRT off to 48 +/- 3 ms at CRT on (p < .001). CPMA was correlated with MAD (r = 0.52, p < 0.05 and r = 0.59, p < 0.05 at CRT off and CRT on, respectively). Moreover, the absolute change in CPMA was correlated with LVESD (r = 0.68) and LVEDD (r = 0.65), both p < 0.05, with the time difference of the basal segments of the septal and lateral wall at CRT on (r = 0.68, p < 0.01), and inversely correlated with LVEF (r = -0.55, p < 0.05). CONCLUSION: In patients with severe LV systolic dysfunction and dilatation CRT was associated with an improvement in both CPMA and MAD.

Adult↗
PubMed2006

Prognostic value of a restrictive mitral filling pattern in patients with systolic heart failure and an implantable cardioverter-defibrillator.

In patients with chronic heart failure and reduced systolic function, an implantable cardioverter-defibrillator (ICD) improves the prognosis, but morbidity and mortality remain high. We attempted to identify the prognostic impact of Doppler echocardiography and QRS duration in such patients. We prospectively enrolled 84 patients with chronic heart failure, an ICD, and impaired systolic function (mean ejection fraction 29 +/- 10%). Echocardiographic measurements included left ventricular dimensions/volumes, ejection fraction, mitral E/A ratio, deceleration time, and tissue Doppler analysis of mitral annular velocities (S', E', A'). A cardiac event (death from pump failure or appropriate ICD therapy, i.e., antitachycardia pacing/shock due to sustained ventricular tachycardia or ventricular fibrillation) was defined as the study end point. During a follow-up of 373 +/- 254 days, 22 patients (26%) had an event (death from pump failure, n = 7; patients who received an appropriate ICD therapy, n = 16). In patients with an event, the QRS duration was longer (169 +/- 41 vs 146 +/- 37 ms, p = 0.023), the mitral E/E' ratio was higher (16.0 +/- 6.5 vs 12.8 +/- 5.9, p = 0.044), and a restrictive filling pattern was more frequent (44% vs 9%, p = 0.017). Stepwise multivariate Cox regression analysis identified a restrictive filling pattern as the only independent predictor of an event (hazard ratio 3.65, 95% confidence interval 1.54 to 8.64, p = 0.003). For patients with a restrictive filling pattern, the outcome was markedly poorer than that for patients with a nonrestrictive pattern (event-free survival rate 38% vs 72%, p = 0.005). In conclusion, in patients with chronic heart failure, an ICD, and systolic dysfunction, a restrictive filling pattern is an independent predictor of adverse cardiac events.

Aged↗
PubMed1993

Evolution of cardiac changes in young insulin-dependent (type 1) diabetic patients--one more piece of the puzzle of diabetic cardiopathy.

Based on our recent reports that increased myocardial contractility has been found in newly diagnosed diabetic patients, and that diastolic (D) dysfunction precedes systolic (S) dysfunction, we suggested that the development of diabetic cardiopathy passes through the following stages: (I) increased myocardial contractility, (II) intact S and D function, (III) intact S function and D dysfunction, and (IV) S and D dysfunction. The aim of this pilot study was to test this hypothesis. One hundred fifty-seven young (26.2 +/- 7.4 years) cardiac-asymptomatic patients with type I diabetes and 54 healthy subjects were studied using M-mode echocardiography. The presence of at least one of the variables for systolic function (ejection fraction, mean velocity of circumference, fiber shortening, and stroke index) or diastolic function [left atrium emptying index (LAEI), EFo slope of anterior mitral leaflet, and isovolumetric relaxation time (IRT)] outside the control mean +/- 2 SD was interpreted as an increased or depressed myocardial contractility, and diastolic dysfunction, respectively. The severity of diabetic complications (retinopathy, nephropathy, and cardiac autonomic neuropathy) was evaluated by the diabetic complication index (DCI = 0 divided by 6 scores). Our hypothesis was confirmed significantly (p < 0.001) in 148 (94%) patients with diabetes. Duration of diabetes and DCI progressed significantly (ANOVA: F = 36.6, p < 0.001; F = 70.8, p < 0.001) with hypothetical stages. Diastolic dysfunction was more pronounced in stage IV than in stage III: IRT (80.5 +/- 18.6 ms vs. 62.5 +/- 16.4, p < 0.001), EFo (63 +/- 15 mm/s vs. 72 +/- 21, p < 0.05), LAEI (0.58 +/- 0.13 vs. 0.8 +/- 0.15, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Echocardiographic detection of early diabetic myocardial disease.

OBJECTIVES: We sought to determine whether disturbances of myocardial contractility and reflectivity could be detected in diabetic patients without overt heart disease and whether these changes were independent and incremental to left ventricular hypertrophy (LVH). BACKGROUND: Left ventricular (LV) dysfunction is associated with diabetes mellitus, but LVH is common in this population and the relationship between diabetic LV dysfunction and LVH is unclear. METHODS: We studied 186 patients with normal ejection fraction and no evidence of CAD: 48 with diabetes mellitus only (DM group), 45 with LVH only (LVH group), 45 with both diabetes and LVH (DH group), and 48 normal controls. Peak strain and strain rate of six walls in apical four-chamber, long-axis, and two-chamber views were evaluated and averaged for each patient. Calibrated integrated backscatter (IB) was assessed by comparison of the septal or posterior wall with pericardial IB intensity. RESULTS: All patient groups (DM, DH, LVH) showed reduced systolic function compared with controls, evidenced by lower peak strain (p < 0.001) and strain rate (p = 0.005). Calibrated IB, signifying myocardial reflectivity, was greater in each patient group than in controls (p < 0.05). Peak strain and strain rate were significantly lower in the DH group than in those in the DM alone (p < 0.03) or LVH alone (p = 0.01) groups. CONCLUSIONS: Diabetic patients without overt heart disease demonstrate evidence of systolic dysfunction and increased myocardial reflectivity. Although these changes are similar to those caused by LVH, they are independent and incremental to the effects of LVH.

Aged↗
PubMed1995

Interrelationship of left ventricular mass, systolic function and diastolic filling in normotensive morbidly obese patients.

OBJECTIVE: To determine the interrelationship of left ventricular (LV) mass, systolic function and diastolic relaxation in morbidly obese subjects. METHOD: We obtained echocardiograms (M-mode, two dimension) and cardiac Doppler studies (pulse wave, continuous wave colour flow) on 50 subjects whose actual body weight was > or = twice ideal body weight. LV mass/height index was calculated from echocardiographic data (Penn Convention). LV systolic function was assessed by calculating LV fractional shortening. LV diastolic filling was assessed by measuring the transmitral Doppler E/A ratio and the transmitral E wave deceleration time. RESULTS: There were significant positive correlations between LV mass/height index and the LV internal dimensions in diastole, systolic blood pressure, LV end-systolic wall wall stress and the transmitral E wave deceleration time. There were significant negative correlations between LV mass/height index and both LV fractional shortening and the transmitral Doppler E/A ratio. There were significant negative correlations between LV fractional shortening and the LV internal dimension in diastole, systolic blood pressure LV end-systolic wall stress and the transmitral E wave deceleration time. There was a significant positive correlation between LV fractional shortening and the transmitral Doppler E/A ratio. There were significant positive correlations between the transmitral E wave deceleration time and LV internal dimension in diastole, systolic blood pressure and LV end-systolic wall stress. There were significant negative correlations between the transmitral Doppler E/A ratio and the aforementioned variables. CONCLUSIONS: Unfavourable alterations in LV loading conditions contribute to the development of LV hypertrophy and impairment systolic dysfunction in morbidly obese subjects. Increasing LV mass and altered loading conditions may synergistically contribute to impairment of LV diastolic filling in such individuals.

Adult↗
PubMed1993

Calcium channel blockers in heart failure.

The rationale for the use of calcium channel blockers in patients with chronic heart failure lies in their vasodilator action, antiischemic effect, ability to lessen left ventricular diastolic dysfunction and data showing their effect in preventing progression of myocardial dysfunction in animals with cardiomyopathy. Despite initial studies reporting improvement of the hemodynamic profile with nifedipine, further evaluation showed variable results, with hemodynamic worsening seen in up to 29% of patients. Longer-term controlled studies evaluating symptoms and clinical status demonstrated worsening chronic heart failure in approximately 25% of patients within 8 weeks of nifedipine therapy. Although diltiazem has a lesser myocardial depressant effect and its short-term use was associated with less frequent hemodynamic and clinical worsening, long-term exposure to the drug in a large group of patients with chronic heart failure due to left ventricular systolic dysfunction after myocardial infarction resulted in an increased incidence of cardiac events, with worsening heart failure and death. The use of verapamil in a similar patient cohort showed the loss of its demonstrated protective effect in patients with clinical evidence of heart failure. In an attempt to improve the safety of calcium channel blockers, the following approaches were suggested: 1) use of second-generation drugs with less myocardial depressant effect; 2) concomitant use of angiotensin-converting enzyme inhibitors to prevent reported neurohormonal activation; and 3) development of drugs with favorable neurohormonal effects. These approaches led to mixed results.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed2000

[Congenital dysplasia of tricuspid valve (Ebstein like) in a 73-year-old male with severe tricuspid insufficiency].

Multiple congenital abnormalities in the structure of the tricuspid valve have been described and, the majority of cases could be considered as variations of Ebstein's anomaly. The onset of the symptoms and the diagnosis depend on the severity of the valve dysfunction and the right ventricular function and size. The age at diagnosis ranges from birth to adulthood, but a delayed diagnosis is rare when tricuspid regurgitation is severe. We cite as an example the case of a 73 year-old male classified as class I of the NYHA up to 5 months before, since then he developed progressive ascitis and edema on his legs. The physical examination suggested severe tricuspid regurgitation. We performed a transtoracic and transesophageal ecocardiogram that showed severe dysplasia in the tricuspid leaflets, severe regurgitation because of lack of adequate joining, dilatation of right chambers and right ventricular systolic dysfunction.

Aged↗
PubMed2003

Reduced hemodynamic load and cardiac hypotrophy in patients with anorexia nervosa.

BACKGROUND: Anorexia nervosa is associated with lower left ventricular mass (LVM) and systolic dysfunction. Whether these abnormalities reflect chronic protein-energy malnutrition or are primarily related to lower cardiac workload is unclear. OBJECTIVE: The objective of the study was to verify whether low LVM in anorexia nervosa is explained by low hemodynamic load. DESIGN: Ninety-one women with anorexia nervosa [macro x +/- SD age: 20.5 +/- 6.1 y; body mass index (in kg/m(2)): 15.6 +/- 1.9; group 1] and 62 normal-weight female control subjects (age: 22.5 +/- 5.5 y; body mass index: 20.9 +/- 1.2; group 2) underwent Doppler echocardiography. LVM was evaluated as the percentage predicted by body height, sex, and stroke work (systolic blood pressure x stroke volume). RESULTS: The left ventricular chamber dimension was smaller and the chamber walls were thinner in group 1 than in group 2, which resulted in significantly lower LVM and LVM indexes (P < 0.0001). Ejection fraction, heart rate, stroke volume, and cardiac output were significantly (P < 0.007) lower in group 1, but peripheral resistance was substantially higher (P < 0.0001). The deviation of LVM from predicted values was lower and the proportion of subjects with inadequate LVM was significantly higher in group 1 than in group 2 (P < 0.0001). This difference was attenuated after adjustment for body weight and heart rate. There were no relations between LVM and laboratory tests in group 1. CONCLUSIONS: Anorexia nervosa is a condition of low hemodynamic load that leads to low LVM. Even with adjustment for stroke work, however, LVM is lower than would be predicted by height, because of the effect of body weight reduction (ie, wasting of lean body mass).

Adult↗
PubMed1997

Effects of aging on left ventricular relaxation in humans. Analysis of left ventricular isovolumic pressure decay.

BACKGROUND: Some experimental studies in animals have shown that myocardial relaxation is prolonged with aging. However, it is not known whether aging alters ventricular isovolumic relaxation in human subjects. METHODS AND RESULTS: We analyzed high-fidelity left ventricular pressures, measured by use of a catheter-tipped manometer, and biplane left ventriculograms in 55 normal subjects who underwent diagnostic cardiac catheterization but who were found to have normal cardiac anatomy and function. There were 38 men and 17 women, ranging in age from 20 to 77 years. Left ventricular isovolumic relaxation was assessed by the exponential time constants of isovolumic pressure decay with (Tb) and without (Tw) an asymptote pressure. Left ventricular volume, ejection fraction, and wall thickness or mass were calculated from left ventricular angiograms. Neither of the time constants of left ventricular relaxation correlated with age (Tb: r = .001 to .10, P = NS: Tw: r = .02 to .05, P = NS). Left ventricular systolic function (ie, ejection fraction and end-systolic volume index), heart rate, and left ventricular wall thickness or mass, which are major hemodynamic determinants of left ventricular relaxation, were not significantly affected by aging. The multivariate analysis of age and hemodynamic variables against the time constants of left ventricular relaxation also indicated that no significant relation was found between age and left ventricular relaxation. CONCLUSIONS: In the absence of coronary artery disease, systemic hypertension, left ventricular systolic dysfunction, or hypertrophy, left ventricular relaxation assessed by the time constant of isovolumic pressure decay remains essentially unchanged with normal adult aging, at least until the eighth decade.

Adult↗
PubMed2006

[Clinical and therapeutic characteristics in patients with heart failure cared for in an internal medicine department].

INTRODUCTION: The Heart Failure (HF) is a very common clinic syndrome in the clinical practise, and a great sanitary social problem. In Spain, it is the main cause of hospitalization in Internal Medicine Services in patients over 65 years old, due to its high comorbidity, in many cases. OBJECTIVE: To determine the profile of admitted patients with HF to an Internal Medicine Service. MATERIAL AND METHODS: It is a retrospective and descriptive study. The following variables were analysed: sex, age, cause of admission, aetiology, risk factors, Framingham diagnostic criteria, type of HF, treatment-on-released, average stay, number of readmissions and the type of ventricular dysfunction (echocardiography). Chi-square test of Pearson or Fisher test were used as statistical methods. P < 0.05 was considered to be statistically relevant. RESULTS: 104 patients were analysed. The percentage of HF was 13.76%. 52.88% were men with an average age of 72.16 +/- 17.78 year. Average age for women was 82.92 +/- 7.24 year. The main cause of admission was dysnea (74%). Hypertension was the principal risk factor (70.13%). When it comes to aetiology, HTA (68.57%) was the main one. Global and left HF (33.65% either) were the most common type of HF. 5.17% of women and 20.69% of men suffered from systolic dysfunction (p < 0.023). 32.76% of women and 41.38% of men had diastolic dysfunction. The base treatment-on-release for the majority of patients consisted of diuretics and digoxin. Patients stayed 15.49 days on average, and the number of readmitted ones came up to 26.67%. CONCLUSIONS: The diagnosis and treatment of HF in an Internal Medicine Service is acceptable. It will be very important to promote the use of beta blockers and angiotensina-converting enzyme inhibitors.

Aged↗
PubMed2006

Alterations in cardiac contractile performance and sarcoplasmic reticulum function in sucrose-fed rats is associated with insulin resistance.

Diabetes mellitus (DM) causes the development of a specific cardiomyopathy that results from the metabolic derangements present in DM and manifests as cardiac contractile dysfunction. Although myocardial dysfunction in Type 1 DM has been associated with defects in the function and regulation of the sarcoplasmic reticulum (SR), very little is known about SR function in Type 2 DM. Accordingly, this study examined whether abnormalities in cardiac contractile performance and SR function occur in the prestage of Type 2 DM (i.e., during insulin resistance). Sucrose feeding was used to induce whole body insulin resistance, whereas cardiac contractile performance was assessed by echocardiography and SR function was measured by SR calcium (Ca(2+)) uptake. Sucrose-fed rats exhibited hyperinsulinemia, hyperglycemia, and hyperlipidemia relative to control rats. Serial echocardiographic assessments in the sucrose-fed rats revealed early abnormalities in diastolic function followed by late systolic dysfunction and concurrent alterations in myocardial structure. The hearts of the 10-wk sucrose-fed rats showed depressed SR function demonstrated by a significant reduction in SR Ca(2+) uptake. The decline in SR Ca(2+) uptake was associated with a significant decrease in the cAMP-dependent protein kinase and Ca(2+)/calmodulin-dependent protein kinase II-mediated phosphorylation of phospholamban. The results show that abnormalities in cardiac contractile performance and SR function occur at an insulin-resistant stage before the manifestation of overt Type 2 DM.

Animals↗
PubMed2004

Patient differences related to management in general practice and the hospital: a cross-sectional study of heart failure in the community.

AIM: To compare patients treated for heart failure in relation to the management in general practices versus hospital admission. METHODS AND RESULTS: Twelve randomly selected general practices (GP) were screened for patients receiving ACE-inhibitor, digoxin, or loop diuretic treatment. The first 500 volunteers of 959 potential subjects were invited to a cardiac examination after exclusion of 235 frail, physically or mentally disabled patients. A diagnosis of heart failure during hospital admission (Hospital-HF, n = 102) was more related (p < 0.05) to male sex (45% vs. 21%), advanced age (73 vs. 70 years), breathlessness (75% vs. 62%), LV systolic dysfunction (47% vs. 20%), objective cardiac abnormality (92% vs. 65%) and higher 4-year mortality (33% vs. 15%) than patients taking loop diuretics due to signs and symptoms of heart failure in GP (GP-HF). Patients without clinical heart failure (n = 301) had the same survival but less symptoms and cardiac abnormalities than GP-HF patients. CONCLUSION: A surplus morbidity and mortality was related to a hospital-based rather than a GP based diagnosis of HF. Patients managed in GP were different from patients entering previous clinical trials of heart failure. We estimate that the pool of patients hospitalised with systolic heart failure would be increased from 1.3 to 1.4 more if all patients from primary care were included.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

A personal perspective on the treatment of heart failure in 1994.

The treatment of heart failure has advanced greatly over the past two decades. Angiotensin-converting enzyme inhibitors have become standard therapy, not only in symptomatic patients but also in those with asymptomatic left ventricular dysfunction. Diuretic regimens have become increasingly potent and sophisticated. Much of the controversy over the efficacy of digoxin has been resolved, although its effect on survival is still uncertain. Most symptomatic patients, therefore, should be treated with what has become "standard" triple therapy, but practices vary as to when and at what dose to use these medications. More problematic is how to treat the patient who remains symptomatic on a three-drug regimen, and how to manage ancillary but important issues such as arrhythmias and thromboembolic risk. This article reflects the author's personal approach to managing the patient with left ventricular systolic dysfunction in 1994.

Cardiac Output, Low↗