Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diastolic Dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed1999

Regional Diastolic Function in Microvascular Angina Studied by Pulsed-Wave Doppler Tissue Imaging.

OBJECTIVES: Diastolic dysfunction is an early finding during myocardial ischemia. However, regional diastolic function has not been studied in patients with microvascular angina (MA). The purpose of this study was to assess the regional diastolic function in patients with MA through use of the new echocardiographic technique, pulsed-wave Doppler tissue imaging (DTI). METHODS: Regional diastolic function was studied by DTI in 81 myocardial segments of seven patients with MA and in 54 segments of six healthy control subjects. RESULTS: Myocardial segments in patients with MA had, in comparison with controls, an increased regional isovolumetric relaxation time (126 +/- 34 vs 99 +/- 34 msec, P < 0.0001), a higher e/a ratio (1.1 +/- 0.7 vs 0.8 +/- 0.3, P = 0.0048), and a lower peak velocity of the late diastolic wave a (6.9 +/- 2.9 vs 8.4 +/- 1.7 cm/msec, P = 0.0009). Moreover, peak velocity of systolic wave s was higher in patients with MA (5.8 +/- 1.4 vs 5.3 +/- 1.2 cm/msec, P = 0.0424). CONCLUSIONS: Patients with MA have an impaired regional diastolic function (an increased regional isovolumetric relaxation time and a lower a wave) and a higher velocity of the regional systolic wave s. These findings may have physiopathological implications.

Journal Article↗
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↗
PubMed1988

[Cardiac and extracardiac parameters as principles in differential therapeutic considerations for decreasing pre- and afterload].

A differential therapy of congestive heart failure requires the identification of the different stages of myocardial damage consequent to the underlying heart disease and the individual adaptive response to it. Because of their different load dependence, it is important to recognize the independent contribution of systolic and diastolic dysfunction in congestive heart failure. The vertical displacement of the diastolic pressure-volume loop is associated with a reduced therapeutic range. Reducing preload may limit the degree of diastolic filling necessary to fill a noncompliant heart and limit active myocardial stretch. The final outcome of any disorder is either to comprise cardiac filling, emptying, or both. When the end-stage is reached, only modification of excessive neurohormonal responses to heart failure remains. Efforts are necessary to avoid substances able to support the maladaptation. The rational use of vasodilator therapy in congestive heart failure is based on the concept that peripheral circulatory mechanisms overshoot, and may thereby act to exacerbate the heart failure. As important as it is to modify late neurohormonal responses, it is even more important to intervene at an earlier stage to reduce the degree of irreversible myocardial damage. Further studies have to prove the potential benefits of ACE-inhibitors in patients with mild heart failure in order to prevent or delay the progress of the disease.

Blood Pressure↗
PubMed1988

[Serial changes in left ventricular configuration and function in hypertrophic cardiomyopathy].

Fifteen patients, 12 males and three females, with hypertrophic cardiomyopathy (HCM) including three of obstructive type (HOCM) were investigated to observe the long-term course of HCM. Left ventriculography and bi-ventriculography were performed twice serially in all cases. We studied the correlations between the serial ECG changes, especially the negative T wave, and the left ventricular configuration, wall thickness, and left ventricular function. Serial ECG changes included: 1) negativity of the T wave which developed or increased concomitantly with increased voltages of SV1 + RV5 (A-1 group: five cases), 2) the negativity decreased or resolved with decreased voltages of SV1 + RV5 (A-2 group: four cases), and 3) insignificant changes of both T waves and SV1 + RV5 (B group: six cases). In the right oblique views at end-diastole, the configuration of the left ventricle was classified in three forms; (1) spade form (S), (2) round form (R), and (3) intermediate form (SR). The results were as follows: 1. The A-1 group showed increased thickness of the apical and anterior walls, but the thickness of the posterior wall and interventricular septal wall did not change serially. In three cases, the thickness of the interventricular septum showed mild hypertrophy at the initial and final observations. The configuration changed from the R or SR form to the S form. Diastolic dysfunction (peak dV/dt/V, peak dV/dt/EDV) was progressive, but end-diastolic volume and ejection fraction did not change. 2. The A-2 group showed the significantly decreased thickness of the apical and anterior walls. The thicknesses of the posterior wall and interventricular septal wall tended to decrease in all cases. In three cases (75%), the interventricular septal wall was markedly hypertrophied on the initial observation. The configuration changed from the S or SR form to the R form. Left ventricular diastolic function and ejection fraction decreased significantly and end-diastolic volume increased. Two cases showed clinical pictures of dilated cardiomyopathy at the final observation. 3. In the B group, there were no marked changes in wall thickness, left ventricular configuration, or systolic and diastolic functions. In conclusion, serial changes in left ventricular configuration, wall thickness, especially of the anterior and apical walls, and left ventricular function were all compatible with the serial changes of the ECG in hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Influence of preload reserve on stroke volume response to exercise in patients with left ventricular systolic dysfunction: a Doppler echocardiographic study.

OBJECTIVES: This study evaluated the role of preload reserve in the stroke volume response to exercise in patients with left ventricular systolic dysfunction by assessing the relation between stroke volume and late left ventricular diastolic filling during exercise. BACKGROUND: In patients with left ventricular diastolic dysfunction, the absence of left ventricular distension is the fundamental mechanism explaining the nonaugmentation of stroke volume during exercise. METHODS: In 32 patients with left ventricular systolic dysfunction and 16 healthy control subjects, mitral and aortic velocities were recorded by Doppler echocardiography at rest and during submaximal supine bicycle exercise. Stroke volume, peak early (E) and late (A) mitral velocities, A/E ratio and end-diastolic filling were measured at rest and during exercise. RESULTS: Stroke volume increased significantly in control subjects but did not change in patients. Peak early mitral velocity increased significantly and to the same extent in both groups, whereas peak late mitral velocity and end-diastolic filling increased significantly in both groups but more so in control subjects; the A/E ratio increased significantly in control subjects but did not change in patients. In addition, stroke volume correlated significantly with peak late mitral velocity during exercise in patients (r = 0.72, p < 0.001). CONCLUSIONS: Compared with control subjects, patients with left ventricular systolic dysfunction exhibited limited increases in both stroke volume and late left ventricular filling during exercise. Furthermore, their stroke volume response correlated with the capacity of the left ventricle to increase late diastolic filling, that is, preload reserve.

Adolescent↗
PubMedDate not supplied

Diagnostic criteria for diastolic heart failure.

A diagnosis of diastolic heart failure can be made if the patient exhibits clinical evidence of heart failure and has a normal left ventricular ejection fraction. The diagnosis is confirmed if there is evidence of ventricular hyperthrophy and/or concentric remodeling, left atrial enlargement, or laboratory evidence of diastolic dysfunction.

Diastole↗
PubMed1999

Progressive cardiac dysfunction and fibrosis in the cardiomyopathic hamster and effects of growth hormone and angiotensin-converting enzyme inhibition.

BACKGROUND: Growth hormone (GH) improves cardiac function in the rat with myocardial infarction, but its effects in a model of primary dilated cardiomyopathy have not been reported. GH effects were examined at early (4 months) and late (10 months) phases of disease in the cardiomyopathic (CM) hamster, and the combination of GH with chronic ACE inhibition was assessed in late-phase heart failure. METHODS AND RESULTS: CM hamsters (CHF 147 line) at 4 months showed severe systolic left ventricular (LV) dysfunction with normal LV filling pressure, and at 10 months there was more severe systolic as well as diastolic dysfunction with increasing myocardial fibrosis. Recombinant human GH alone for 3 weeks at age 4 months increased LV wall thickness and reduced systolic wall stress without altering diastolic wall stress, whereas at 10 months, wall stress and fractional shortening did not improve. The LV dP/dt(max) was enhanced at both ages by GH, which at 4 months reflected increased contractility, but at 10 months was most likely caused by elevation of the LV filling pressure. The increasing degree of fibrosis correlated inversely with LV function but was unaffected by GH. In other CM hamsters, high-dose ACE inhibition alone (quinapril), started at 8 months and continued for 11 weeks, improved LV function and inhibited unfavorable remodeling, but the addition of GH for 3 weeks at age 10 months produced increased wall thickness with little additional functional benefit and increased the LV filling pressure and diastolic wall stress. CONCLUSIONS: GH treatment alone improved LV dysfunction at 4 months of age in CM hamsters by increasing contractility and reducing wall stress but had few beneficial effects at 10 months in severe LV failure. After chronic ACE inhibition, addition of GH at 10 months had no additional beneficial effects and further increased LV diastolic pressure. These differing effects of GH may relate to the progressive increase of LV fibrosis in the CM hamster.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Clinical syndrome suggestive of heart failure is frequently attributable to non-cardiac disorders--population-based study.

AIM: To assess how often the clinical syndrome (CS) of heart failure is attributable to alternative, including non-cardiac, explanations. METHODS AND RESULTS: Cross-sectional evaluation of 739 community participants aged>or=45 years. Subjects with >or=2 symptoms or signs (dyspnoea or fatigue, orthopnoea, nocturnal paroxysmal dyspnoea, third heart sound, jugular venous distension, rales and lower limb oedema) or who were receiving loop diuretics were considered to have the clinical syndrome of heart failure. Attributable fractions were derived based on adjusted odds ratios and the prevalence of underlying disorders among cases. CS was present in 28.0% of women and in 15.2% of men, p<0.001. The multivariate-adjusted fraction of CS attributable to female gender was 40.6%, to age>or=65 years 28.5%, left ventricular systolic dysfunction, left ventricular dilatation or moderate-severe valvular disease 4.9%, diastolic dysfunction or atrial fibrillation 13.0%, obesity 22.6%, coronary heart disease 7.2% and chronic lung disease 6.9%. When additionally adjusting for depressive symptoms, the association with gender and age became much weaker, and 32% of cases were attributable to depressive symptoms. Forty-two percent of subjects with CS had cardiac abnormalities. CONCLUSION: In less than half of subjects with CS was systolic or diastolic heart failure confirmed. Female gender, older age, obesity and depressive symptoms accounted for the largest fraction of CS.

Age Factors↗
PubMed2003

Left ventricular isovolumic relaxation is a predictor of left ventricular end-diastolic pressure.

BACKGROUND: The relationship between isovolumic left ventricular (LV) relaxation and LV filling pressures remains incompletely explored. If there is a relationship between the rate of early diastolic LV relaxation and LV end-diastolic pressure, this would have important implications concerning both our understanding and, potentially, our treatment of LV diastolic dysfunction. OBJECTIVE: To examine the baseline hemodynamic correlates of LV end-diastolic pressure in patients with both normal and abnormal LV function. METHODS: The relationships between LV end-diastolic pressure, a variety of hemodynamic parameters (tau, the rate of LV isovolumic relaxation, LV peak positive+dP/dt, LV peak systolic pressure and heart rate), measures of LV end-systolic and end-diastolic volume, and age were determined using regression analysis techniques in 104 patients with normal LV systolic function and 90 patients with an LV ejection fraction of less than 40%. RESULTS: Univariate analysis demonstrated a correlation between tau and LV end-diastolic pressure (r=0.743, P<0.001). There were significant univariate relationships between a number of other hemodynamic variables and LV end-diastolic pressure. A multiple regression model demonstrated that tau made the most important contribution to a model where LV end-diastolic pressure is the dependent variable. LV peak systolic pressure and heart rate also made significant contributions to the model. In 33 of these patients, when LV end-diastolic pressure was reduced using an inferior vena cava occlusion balloon, tau did not change. The acute administration of clonidine (n=11) caused an increase in LV end-diastolic pressure that was closely correlated with an observed increase in tau (r=0.843, P<0.001). CONCLUSIONS: These observations suggest that the rate of LV isovolumic relaxation is a predictor of LV end-diastolic pressure.

Cardiac Catheterization↗
PubMed2004

Renal insufficiency and heart failure: prognostic and therapeutic implications from a prospective cohort study.

BACKGROUND: The prevalence, prognostic import, and impact of renal insufficiency on the benefits of ACE inhibitors and beta-blockers in community-dwelling patients with heart failure are uncertain. METHODS AND RESULTS: We analyzed data from a prospective cohort of 754 patients with heart failure who had ejection fraction, serum creatinine, and weight measured at baseline. Median age was 69 years, and 43% had an ejection fraction > or =35%. By the Cockcroft-Gault equation, 118 patients (16%) had creatinine clearances < or =30 mL/min and 301 (40%) had creatinine clearances between 30 and 59 mL/min. During follow-up (median 926 days), 385 patients (37%) died. Even after adjustment for all other prognostic factors, survival was significantly associated with renal function (P=0.002) in patients with either systolic or diastolic dysfunction; patients exhibited a 1% increase in mortality for each 1-mL/min decrease in creatinine clearance. The associations with 1-year mortality reductions were similar for ACE inhibitors (OR 0.46 [95% CI 0.26 to 0.82] versus OR 0.28 [95% CI 0.11 to 0.70]) and beta-blockers (OR 0.40 [95% CI 0.23 to 0.70] versus OR 0.41 [95% CI 0.19 to 0.85]) in patients with creatinine clearances <60 mL/min versus > or =60 mL/min, although these drugs were used less frequently in patients with renal insufficiency. CONCLUSIONS: Renal insufficiency is more prevalent in patients with heart failure than previously reported and is an independent prognostic factor in diastolic and systolic dysfunction. ACE inhibitors and beta-blockers were associated with similar reductions in mortality in patients with and without renal insufficiency.

Adrenergic beta-Antagonists↗
PubMed2004

Mitral regurgitation in patients with advanced systolic heart failure.

BACKGROUND: Mitral regurgitation (MR) may develop in patients with advanced systolic congestive heart failure (CHF) without organic mitral valve disease and contribute to worsening symptoms and survival. Surgical mitral annuloplasty improves symptoms in patients with advanced CHF, and percutaneous approaches to mitral annuloplasty are being developed. Our objective was to define the prevalence, clinical correlates, and prognostic implications of functional MR and the use of mitral annuloplasty in patients with advanced systolic CHF evaluated in a heart failure clinic. METHODS AND RESULTS: We reviewed clinical, echocardiographic, and survival data from all patients with advanced systolic CHF (New York Heart Association class III or IV; ejection fraction </=35%) resulting from ischemic or idiopathic cardiomyopathy who were evaluated at our heart failure clinic between January 1996 and September 2001. Of 716 patients with advanced CHF, 558 had satisfactory baseline echocardiograms performed at our institution. Among these patients, MR was severe in 24 (4.3%), moderate-severe in 70 (12.5%), moderate in 122 (21.9%), mild-moderate in 66 (11.8%), mild in 218 (39.1%), and absent or present as only a trace in 58 (10.4%). The severity of MR was confirmed by quantitative analysis in 72% of patients with hemodynamically significant MR (more than moderate). The severity of MR correlated with the severity of systolic dysfunction (P <.001), ventricular dilatation (P <.03), atrial dilatation (P <.001), diastolic dysfunction (P <.001), and pulmonary hypertension (P <.001). Coexistent severe or moderate-severe tricuspid regurgitation was present in 25% of patients with hemodynamically significant MR. Patients with hemodynamically significant MR had higher mortality (P=.03) but not when controlling for age, sex, cause, New York Heart Association class, and ejection fraction (P=.95). Only 3 patients subsequently underwent mitral valve repair. CONCLUSION: Among patients with advanced CHF, hemodynamically significant MR is common. The severity of MR did not provide independent prognostic information in this group recognized to have uniformly high mortality.

Aged↗
PubMed2000

A rationale for the use of beta-blockers as standard treatment for heart failure.

BACKGROUND: Cardiac sympathetic activation is one of the major and earlier changes observed in patients with heart failure. Its relation to the severity of the disease and its independent prognostic value show that it may directly contribute to the progression of heart failure. beta-Blockers are the most effective tool to counteract the untoward effects of sympathetic activation on the cardiovascular system. METHODS AND RESULTS: We reviewed the results of the placebo-controlled, double-blind studies about the effects of beta-blockers in patients with heart failure. These studies have involved almost 10,000 patients to date and have consistently shown that the long-term administration of beta-blockers is associated with a highly significant improvement in both left ventricular function and prognosis of the patients with heart failure. The evidence supporting the use of beta-blockers now equals or even surpasses that of angiotensin-converting enzyme inhibitors; therefore beta-blockers should be considered part of standard therapy. Issues that remain unclarified include the mechanisms through which beta-blockers may improve cardiac function and their tolerability and efficacy in specific groups of patients (such as those with asymptomatic left ventricular dysfunction, severe heart failure, the elderly, or those with left ventricular diastolic dysfunction). It is not currently clear whether the pharmacologic differences between individual beta-blockers are clinically relevant. If they are, the potential for even greater benefit with certain agents exists. It is hoped that these issues will be clarified by the results of ongoing multicenter trials.

Adrenergic beta-Antagonists↗
PubMed1999

Influence of left ventricular cavity size on clinical presentation in hypertrophic cardiomyopathy.

The aim of this study was to assess whether left ventricular (LV) cavity size relates to functional impairment and syncope in patients with hypertrophic cardiomyopathy (HC). LV diastolic dysfunction influences functional limitation in HC. A reduced LV end-diastolic dimension may underlie impaired diastolic properties and be implicated in hemodynamic syncope. Eighty-two consecutive patients with HC (off drugs, in sinus rhythm) underwent echocardiography to measure LV end-diastolic dimension in the short-axis view (indexed to the body surface area) and radionuclide angiography (n = 50) to calculate peak filling rate (normalized to stroke counts/s). Patients in New York Heart Association functional classes II to IV had smaller LV end-diastolic dimension (23.2 +/- 2.6 vs 25.5 +/- 2.5 mm/M2, p = 0.0001) and lower peak filling rate (4.3 +/- 1.4 vs 5.1 +/- 1.3 stroke counts/s, p = 0.036) than those in New York Heart Association class I. LV end-diastolic diameter was correlated to peak filling rate (r = 0.37; p = 0.008). The most potent predictors of functional limitation were LV end-diastolic dimension (relative risk [RR] 0.63, confidence interval [CI] 0.45 to 0.88; p = 0.008), age (RR 1.09, CI 1.03 to 1.17; p = 0.003), and LV thickness score (RR 1.08, CI 1.02 to 1.13; p = 0.003). LV cavity size was smaller in patients with functional limitation irrespective of obstruction and hypertrophy. Patients with differed from those without a history of syncope for a smaller LV end-diastolic dimension (23.2 +/- 2.5 vs 25.0 +/- 2.7 mm/M2, p = 0.008), which was the only independent predictor of syncope (RR 0.77, CI 0.63 to 0.95; p = 0.013). Thus, a small LV cavity size is associated with functional limitation and history of syncope in HC.

Adolescent↗
PubMed2000

Left ventricular systolic dysfunction during exercise and dobutamine stress in patients with hypertrophic cardiomyopathy.

OBJECTIVES: We sought to characterize stress-induced left ventricular systolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: Myocardial ischemia and diastolic dysfunction occur in patients with HCM. We hypothesized that, in the setting of transient myocardial ischemia, left ventricular systolic dysfunction occurs during exercise and dobutamine stress. METHODS: We studied 39 patients with HCM but without obstructive symptoms at rest or coronary artery disease. A continuous ventricular function monitor equipped with cadmium telluride detectors (VEST) was used to evaluate left ventricular function during supine bicycle ergometer exercise. Dobutamine stress echocardiography (DSE) was also performed. The left ventricular ejection fraction (LVEF) and regional wall motion were determined from echocardiographic images. RESULTS: Changes in the LVEF correlated between exercise and dobutamine stress (r = 0.643, p < 0.0001). The LVEF decreased more than 5% at peak exercise in 17 of patients (group II), while the other patients had normal responses (group I). New regional wall motion abnormalities during dobutamine infusion were detected in 18 of 110 (16.4%) segments in group I and 42 of 85 (49.4%) segments in group II. Decreased or unchanged regional wall motion occurred more frequently in hypertrophied segments than in nonhypertrophied segments (p < 0.0001). There were significant inverse correlations between the LVEF responses during both stresses and the number of abnormal segments noted during dobutamine stress in all patients (VEST: p < 0.005; DSE: p < 0.0005). Signs of left ventricular obstruction were observed in 11 of 39 patients during DSE. However, there was no significant correlation between the LVEF response and the dobutamine-induced left ventricular pressure gradient. CONCLUSIONS: Exercise-induced systolic dysfunction occurred in 50% of patients with HCM. In these patients, regional wall motion abnormalities were present in hypertrophied segments.

Adult↗
PubMed1989

Effects of long-term antihypertensive treatment with tertatolol on diastolic function in hypertensive patients with and without left ventricular hypertrophy.

UNLABELLED: We assessed the effects of long-term antihypertensive treatment with 5 mg tertatolol, a noncardioselective beta-blocker, on left ventricular hypertrophy (LVH) and diastolic function. Fifteen hypertensive patients were selected as good responders to previous treatment with tertatolol (supine blood pressure less than 140/90 mm Hg). They were divided into 2 groups: group 1 with LVH (n = 6) and group 2 without LVH (n = 9). After a one month wash-out period, all patients received 5 mg tertatolol once daily. In case of uncontrolled blood pressure (BP), the dose was doubled after 2 weeks in 10 patients. BP control was obtained in all patients. M-mode echocardiography and Doppler-echocardiography were performed under controlled conditions after BP normalization and after 6 months of treatment. Long-term BP normalization significantly reduced left ventricular mass index (LVMI) in group 1 (from 137 +/- 3 to 121 +/- 3 g/m2, P less than .01), but not in group 2 (from 120 +/- 3 to 114 +/- 4 g/m2, P = NS). After 2 weeks of effective therapy, the ratio between early and late diastolic peak flow velocity across the mitral valve (E/A ratio), significantly increased in both groups (from 0.72 +/- 0.04 to 0.87 +/- 0.06 in group 1, P less than .05; and from 1.13 +/- 0.06 to 1.26 +/- 0.07 in group 2, P less than .05). After 6 months, together with the reduction of LVMI, a further increase of E/A ratio was only observed in group 1 (to 1.30 +/- 0.12, P less than .05). IN CONCLUSION: (1) LVH contributes to left ventricular diastolic dysfunction in hypertensive patients since its reversal is able to improve diastolic filling, and (2) effective antihypertensive treatment with tertatolol improves diastolic function independently from its effect on LV mass.

Adrenergic beta-Antagonists↗
PubMed2006

Long-term cardiac follow-up in survivors of a malignant bone tumour.

BACKGROUND: Longitudinal studies of cardiac function in long-term childhood cancer survivors are scarce and frequently concern a median follow-up shorter than 13 years. PATIENTS AND METHODS: Cardiac assessment was performed in 22 doxorubicin-treated long-term survivors of a malignant bone tumour at median 22 years (range 15-27.5) post-treatment. Age at follow-up was 39 years (range 27-59) and cumulative dose of doxorubicin was 360 mg/m(2) (range 225-550). Cardiac function was assessed by echocardiography and (24-h) ECG. The results were compared with those of earlier assessments at 9 years (1992) and 14 years (1997) post-treatment. RESULTS: Systolic dysfunction was found in 27% (9% in 1997; P = 0.02) and diastolic dysfunction in 45% (18% in 1997; P = 0.02). Heart rate variability showed further deterioration compared with earlier results. CONCLUSIONS: Twenty-two years after doxorubicin-treatment, bone tumour survivors showed progressive cardiac dysfunction.

Adolescent↗
PubMed2006

Cardioprotective effects of acute and chronic opioid treatment are mediated via different signaling pathways.

A 5-day exposure to morphine exerts a profound cardioprotective phenotype in murine hearts. In the present study, we examined mechanisms by which morphine generates this effect, exploring the roles of G(i) and G(s) proteins, PKA, PKC, and beta-adrenergic receptors (beta-AR) in acute and chronic opioid preconditioning. Langendorff-perfused hearts from placebo, acute morphine (AM; 10 micromol/l)-, or chronic morphine (CM)-treated mice (75-mg pellet, 5 days) underwent 25-min ischemia and 45-min reperfusion. After reperfusion, placebo-treated hearts exhibited marked contractile and diastolic dysfunction [rate-pressure product (RPP), 40 +/- 4% baseline; end-diastolic pressure (EDP), 33 +/- 3 mmHg], whereas AM hearts showed significant improvement in recovery of RPP and EDP (60 +/- 3% and 23 +/- 4 mmHg, respectively; P < 0.05 vs. placebo). Furthermore, CM hearts demonstrated a complete return of diastolic function and significantly greater recovery of contractile function (83 +/- 3%, P < 0.05 vs. both placebo and AM). Pretreatment with G(i) protein inhibitor pertussis toxin abolished AM protection while partially attenuating CM recovery (P < 0.05 vs. placebo). Treatment with G(s) inhibitor NF-449 did not affect AM preconditioning yet completely abrogated CM preconditioning. Similarly, PKA inhibition significantly attenuated the ischemia-tolerant state afforded by CM, whereas it was ineffective in AM hearts. PKC inhibition with chelerythrine was ineffective in CM hearts while completely abrogating AM preconditioning. Moreover, whereas beta(1)-AR blockade with CGP-20712A failed to alter recovery in CM hearts, the beta(2)-AR antagonist ICI-118,551 significantly attenuated postischemic recovery. These data describe novel findings whereby CM preconditioning is mediated by a PKC-independent pathway involving PKA, beta(2)-AR, and G(s) proteins, whereas AM preconditioning is mediated via G(i) proteins and PKC.

Analgesics, Opioid↗
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↗