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PubMed1997

Antihypertensive therapy. Angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, and calcium antagonists.

ACEIs, angiotensin II receptor antagonists, and calcium antagonists are effective and well-tolerated antihypertensive agents but, except in special situations, should be considered alternative drugs for first line therapy until randomized trials show that they are at least as effective as diuretics and beta-blockers in preventing cardiovascular morbidity and mortality for a broad spectrum of hypertensive patients. ACEIs are particularly indicated for managing patients with congestive heart failure due to systolic dysfunction and patients with diabetic nephropathy, especially in Type I diabetes. Theoretically, the AII receptor antagonists will be equally effective for these indications, and randomized trials are now underway to demonstrate this. Special indications for calcium antagonists in the management of hypertension include angina pectoris, and for the non-dihydropyridine calcium antagonists, paroxysmal supraventricular tachycardia, and atrial fibrillation with rapid ventricular rate. Isolated systolic hypertension in the elderly is a special indication for long-acting dihydropyridine calcium antagonists, although diuretics are preferred. Calcium antagonists have been particularly effective in managing hypertension induced by cyclosporine. They are contraindicated in CHF due to systolic dysfunction and in the management of acute myocardial infarction. The long-term cardioprotective effect of calcium antagonists after a myocardial infarction has been demonstrated only for verapamil and diltiazem in patients with no evidence of LV dysfunction during their infarction. Calcium antagonists should be prescribed for this purpose only when beta-blockers are poorly-tolerated or contraindicated.

Angiotensin Receptor Antagonists↗
PubMed2001

The pathogenesis of acute pulmonary edema associated with hypertension.

BACKGROUND: Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both. METHODS: We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment. RESULTS: The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode. CONCLUSIONS: In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation.

Acute Disease↗
PubMed2005

Clinical update: the role of angiotensin II receptor blockers in patients with left ventricular dysfunction (Part II of II).

Almost 5 million individuals in the United States have chronic heart failure (HF), which is increasing in prevalence. Angiotensin-converting enzyme (ACE) inhibitors are standard therapies for HF, although more than 10% of patients with HF are unable to tolerate these agents. Furthermore, ACE inhibitors may not provide complete blockade of the renin-angiotensin system (RAS) in the long term. Because angiotensin II receptor blockers (ARBs) may block the RAS more completely than ACE inhibitors and are better tolerated, several large-scale ARB trials have been performed exploring their potential role in treating patients with symptomatic HF and left ventricular systolic dysfunction. The Losartan Heart Failure Survival Study (ELITE II) demonstrated no significant differences in morbidity and mortality between the ARB losartan and the ACE inhibitor captopril among elderly patients with HF. The Valsartan Heart Failure Trial (Val-HeFT) demonstrated reductions in hospitalizations for HF with the ARB valsartan when added to standard HF therapy, with no effect on mortality. Both trials suggested a potential negative interaction between ARB and beta-blocker therapy. The Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) program demonstrated significant reductions in morbidity and mortality with the ARB candesartan in patients with HF due to systolic dysfunction, with or without ACE inhibitors and with or without beta blockers. Thus, the addition of ARBs to the treatment regimen of patients with symptomatic HF should be strongly considered.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1996

Noninvasive doppler echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: a simultaneous Doppler echocardiographic and cardiac catheterization study.

OBJECTIVES: The purpose of this study was to examine the relation of the mitral flow velocity curves to left ventricular filling pressures in patients with two different types of myocardial problems: hypertrophic cardiomyopathy and severe left ventricular systolic dysfunction. BACKGROUND: Previous studies have suggested that assessment of Doppler-derived mitral flow velocity curves can be used to predict left ventricular filling pressures in specific disease entities. However, it is unclear whether information derived from specific mitral flow velocity curves obtained from one disease entity can be valid in other disease states. METHODS: The study group consisted of 42 patients with left ventricular systolic dysfunction (group A) and 55 patients with hypertrophic cardiomyopathy (group B); both groups underwent simultaneous cardiac catheterization and were studied by Doppler echocardiography. High fidelity measures of left atrial and left ventricular pressures were obtained simultaneously with mitral flow velocity curves. RESULTS: There was a significant relation between the Doppler echocardiographic variables and mean left atrial pressure in group A patients. The left atrial pressure was directly related to the E/A ratio (r = 0.49, p = 0.004) and inversely related to the deceleration time (r = 0.73, p < 0.001). The sensitivity and specificity of the deceleration time, < 180 m/s, which indicated a mean left atrial pressure > or = 20 mm Hg, were both 100%. In group B patients, there was no significant relation between mean left atrial pressure and deceleration time. CONCLUSIONS: Doppler echocardiographic mitral flow velocity curves are useful in predicting and estimating left ventricular filling pressures in patients with left ventricular dysfunction. However, because of the complexity of the multiple interrelated factors that determine diastolic filling of the left ventricle, these flow velocity curves cannot be used in patients with other disease entities, such as hypertrophic cardiomyopathy. Future studies of different disease states are necessary to fully understand the role of Doppler echocardiography in the assessment of diastolic filling.

Adult↗
PubMed2004

Clinical trials update and cumulative meta-analyses from the American College of Cardiology: WATCH, SCD-HeFT, DINAMIT, CASINO, INSPIRE, STRATUS-US, RIO-Lipids and cardiac resynchronisation therapy in heart failure.

This article continues a series of reports on recent research developments in the field of heart failure. Key presentations made at the American College of Cardiology meeting, held in New Orleans, Louisiana, USA in March 2004 are reported. These new data have been added to existing data in cumulative meta-analyses. The WATCH study randomised 1587 patients with heart failure and left ventricular systolic dysfunction to warfarin, aspirin or clopidogrel. The study showed no difference between the effects of these agents on mortality or myocardial infarction, but hospitalisations for heart failure were higher on aspirin (22.2%) compared to warfarin (16.1%). The SCD-HeFT study showed that ICD therapy reduced all-cause mortality at 5 years by 23% in patients with predominantly NYHA class II heart failure and left ventricular systolic dysfunction, but amiodarone was ineffective. The DINAMIT study showed that ICD therapy was not beneficial in patients with left ventricular dysfunction after a recent MI, even in those with risk factors for arrhythmic death. In CASINO, levosimendan improved survival compared with dobutamine or placebo in patients with decompensated heart failure. INSPIRE showed that SPECT imaging can be used to assess risk early after acute MI safely and accurately. Rimonabant was shown to be safe and effective in treating the combined cardiovascular risk factors of smoking and obesity. An overview of new developments in cardiac resynchronisation therapy (CRT) in heart failure is also reported.

Anticoagulants↗
PubMed2000

Optimising direct access ECHO referral in suspected heart failure.

The objective was to prospectively validate a method of increasing the sensitivity, specificity and negative predictive value of a normal ECG in the exclusion of left ventricular systolic dysfunction by the addition of clinical history. We performed a prospective three year study of all referrals to our direct access ECHO service for assessment of LV function. The ECG was reported blind of the result of the ECHO, history of MI or not was noted, and result of the ECHO predicted. Over three years 416 patients were assessed for the presence or absence of left ventricular systolic dysfunction and consequent changes in clinical management. A total of 320(77%) of patients referred with suspected left ventricular dysfunction were found to have normal left ventricular function. Of the 250(60%) patients treated prior to referral for assessment, 183(73%) were treated inappropriately. The combination of a normal ECG and a negative history of myocardial infarction had a sensitivity of 98% and a negative predictive value of 99% in the assessment of LV function. This was an improvement over a normal ECG alone. Our study shows that diagnosis and treatment of heart failure in the community remains sub-optimal. The combination of a normal ECG and no previous history of myocardial infarction is shown to be a sensitive and accurate predictor of normal left ventricular function. If adopted by general practitioners this would be a valuable method of optimising the use of echocardiography in patients with suspected left ventricular dysfunction.

Echocardiography↗
PubMed2007

Can late gadolinium enhancement by cardiovascular magnetic resonance identify coronary artery disease as the etiology of new onset congestive heart failure?

BACKGROUND: New left ventricular systolic dysfunction affects 500,000 Americans and coronary artery disease (CAD) is responsible for two-thirds of cases. Identifying CAD has both prognostic and therapeutic implications. We evaluated the ability of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance imaging (CMR) to detect CAD as the etiology of recent onset congestive heart failure (CHF). METHODS: CMR and LGE were performed in 26 patients with new onset left ventricular systolic dysfunction. All patients received an x-ray angiography for identification of CAD. Patients with an acute coronary syndrome with troponin I > 1.0 ng/ml or a history of CAD were excluded. The presence and distribution of LGE was evaluated. RESULTS: Significant coronary stenoses were present in 5 of 26 patients (19%). LGE in an infarct pattern was found in 2 of the 5 patients with CAD. Of the 21 patients without CAD, 2 had midwall enhancement but none had evidence of LGE in an infarct pattern. CONCLUSIONS: When present, LGE in an infarct pattern suggests CAD as the etiology of new onset CHF. However, the absence of LGE does not exclude CAD as the underlying etiology. A small proportion of patients with a nonischemic cause of new onset CHF have LGE limited to the midwall.

Adult↗
PubMedDate not supplied

[Repeated cerebral infarction in a patient with Duchenne's muscular dystrophy].

INTRODUCTION: We describe a case of Duchenne muscular dystrophy (DMD) with multiple strokes related to dilated cardiomyopathy. CASE REPORT: A 13 year old boy, with advanced stage DMD was admitted to the hospital because of acute motor and sensory impairment in his right bodyside. Imaging study revealed lesions in basal ganglia and prerolandic cortex in the left hemisphere that were compatible with infarcts in the territory of the medial cerebral artery. Cardiologic evaluation revealed dilation of the left ventriculi and systolic dysfunction with ejection fraction of 35 40%. The symptoms evolved to a residual right hemiparesia. Five months later, the patient developed a transient episode of aphasia and the study performed in this case revealed lesions compatible with infarcts in basal ganglia and insular cortex of the right cerebral hemisphere. CONCLUSION: Cerebral infarction related to cardiomyopathy can worsen the clinical condition of patients with DMD. Early treatment of dilated cardiomyopathy with systolic dysfunction, including use of antithrombotic agents to prevent cerebrovascular complications, could help to improve the course of the disease.

Adolescent↗
PubMed2006

Peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a rare cardiac disorder of unknown cause that occurs in pregnant females, most commonly in the early postpartum period. It shares many clinical characteristics with idiopathic dilated cardiomyopathy but occurs at a younger age and is associated with a better prognosis. The etiology and pathogenic mechanisms have been difficult to study, however current hypotheses include infectious, immunologic, nutritional, and iatrogenic causes. Diagnosis is based upon the clinical presentation of congestive heart failure and objective evidence of left ventricular systolic dysfunction. Mortality rates over the past 10 years in PPCM have decreased, most likely due to advances in medical therapy for heart failure and use of implantable defibrillators. For those patients, who remain refractory to conventional pharmacologic therapy, cardiac transplantation and mechanical circulatory support are viable options. In less than 50% of PPCM patients, left ventricular function normalizes with pharmacologic therapy. However, subsequent pregnancies are often associated with recurrence of left ventricular systolic dysfunction.

Cardiomyopathies↗
PubMed2000

Diastolic heart failure.

Primary diastolic failure is typically seen in patients with hypertensive or valvular heart disease as well as in hypertrophic or restrictive cardiomyopathy but can also occur in a variety of clinical disorders, especially tachycardia and ischemia. Diastolic dysfunction has a particularly high prevalence in elderly patients and is generally associated, with low mortality but high morbidity. The pathophysiology of diastolic dysfunction includes delayed relaxation, impaired LV filling and/or increased stiffness. These conditions result typically in an upward displacement of the diastolic pressure-volume relationship with increased end-diastolic, left atrial and pulmo-capillary wedge pressure leading to symptoms of pulmonary congestion. Diagnosis of diastolic heart failure requires three conditions: (1) presence of signs or symptoms of heart failure; (2) presence of normal or slightly reduced LV ejection fraction (EF > 50%) and (3) presence of increased diastolic filling pressure. Assessment of diastolic function can be performed with several non-invasive (2D- and Doppler-echocardiography, color Doppler M-mode, Doppler tissue imaging, MR-myocardial tagging, radionuclide ventriculography) and invasive techniques (micromanometry, angiography, conductance method). Doppler-echocardiography is the most useful tool to routinely measure diastolic function. Different techniques can be used alone or in combination to assess LV diastolic function, but most of them are dependent on heart rate, pre- and afterload. The transmitral flow pattern remains the starting point, since it is easy to acquire and rapidly categorizes patients into normal (E > A), delayed relaxation (E < A), and restrictive (E >> A) filling patterns. Invasive assessment of diastolic function allows determination of the time constant of relaxation from the exponential pressure decay during isovolumic relaxation, and the evaluation of the passive elastic properties from the slope of the diastolic pressure-volume (= constant of chamber stiffness) and stress-strain relationship (= constant of myocardial stiffness). The prognosis of diastolic heart failure is usually better than for systolic dysfunction. Diastolic heart failure is associated with a lower annual mortality rate of approximately 8% as compared to annual mortality of 19% in heart failure with systolic dysfunction, however, morbidity rate can be substantial. Thus, diastolic heart failure is an important clinical disorder mainly seen in the elderly patients with hypertensive heart disease. Early recognition and appropriate therapy of diastolic dysfunction is advisable to prevent further progression to diastolic heart failure and death. There is no specific therapy to improve LV diastolic function directly. Medical therapy of diastolic dysfunction is often empirical and lacks clear-cut pathophysiologic concepts. Nevertheless, there is growing evidence that calcium channel blockers, beta-blockers, ACE-inhibitors and AT2-blockers as well as nitric oxide donors can be beneficial. Treatment of the underlying disease is currently the most important therapeutic approach.

Cardiac Catheterization↗
PubMedDate not supplied

Effect of long-term hyperhomocysteinemia on myocardial structure and function in hypertensive rats.

BACKGROUND: Postulated mechanisms of hyperhomocysteinemia (Hhe) overlap with proposed mechanisms of adverse cardiac remodeling such as altered collagen metabolism and oxidant stress. Hence we examined the hypothesis that Hhe would promote myocardial fibrosis and systolic dysfunction. METHODS: Three-month-old spontaneously hypertensive rats (SHRs) were divided into three groups: (1) control, given amino-acid defined diet for 20 weeks; (2) Hhe group, given Hhe-inducing diet for 20 weeks; and (3) combined diet group, which were given Hhe-inducing diet for 10 weeks (which leads to myocardial fibrosis and diastolic dysfunction as shown in our prior studies) and subsequently returned to amino acid-defined diet for 10 more weeks. At the end of the treatment period, plasma homocysteine (Hcy) levels and blood pressure were measured, and hearts were isolated for histomorphometric and biochemical assessment of cardiac remodeling and myocardial oxidative stress, and for in vitro cardiac function studies. RESULTS: The Hhe animals demonstrated a significant increase in the ratio of collagenous to noncollagenous protein due to reactive interstitial fibrosis, and increased myocardial oxidant stress, compared to the control group. Systolic function was significantly depressed in the Hhe animals compared to the control group. These changes were partially prevented by return to control diet at 10 weeks. CONCLUSIONS: Our results demonstrate that clinically relevant levels of Hhe accelerate progression of hypertensive heart disease to systolic dysfunction and that increased myocardial oxidant stress may play a role in this process. Considering the high prevalence of hypertension and Hhe in the general population, our findings may have great clinical significance.

Animals↗
PubMed2002

Effects of chronic, rapid right atrial pacing on cardiac hemodynamics and myofibrillar ATPase activity in piglets.

OBJECTIVES: To determine whether chronic, rapid right atrial pacing in newborn neonatal piglets has any effects on cardiac hemodynamics, and whether these changes are associated with intrinsic alterations in cardiac contractile potential as shown by cardiac myofibrillar calcium ATPase activity. BACKGROUND: Although many studies have examined aspects of heart function in models of supraventricular tachycardia, far less is known about its effects in neonatal animals. It is thought that rapid pacing induces a dilated cardiomyopathy in immature pigs. ANIMALS AND METHODS: Two-week-old piglets underwent rapid right atrial pacing (250 beats/min) for 10 days, and their cardiac hemodynamic response was monitored. To obtain subcellular mechanistic information regarding systolic dysfunction, cardiac myofibrils were isolated and calcium adenosine triphosphatase activity was measured. RESULTS: Control piglets had a heart rate of 185 beats/min at the end of the experimental period. Pulmonary artery flow, pulmonary artery flow index and left ventricular end-diastolic diameter were unchanged as a function of rapid, chronic right atrial pacing. Aortic pressure decreased in the paced piglets. Left atrial pressure increased approximately threefold in the paced animals. Left ventricular end-systolic diameter was also significantly higher after pacing, but left ventricular end-diastolic diameter was unchanged. Left ventricular shortening fraction was depressed approximately 50%. Myofibrillar calcium adenosine triphosphatase activity was significantly depressed as a function of pacing. CONCLUSIONS: Neonatal piglets undergoing chronic supraventricular tachycardia exhibit systolic dysfunction in the absence of dilation. The depression in contractile protein calcium adenosine triphosphatase activity provides information at a subcellular level regarding the mechanism responsible for this cardiomyopathy.

Adenosine Triphosphatases↗
PubMed1994

Management of heart failure. II. Counseling, education, and lifestyle modifications.

OBJECTIVE: This article reviews the role of counseling, education, dietary modifications, and exercise for patients with heart failure due to left ventricular systolic dysfunction. DATA SOURCE: We reviewed studies published in English between 1966 and 1993 and referenced in MEDLINE or EMBASE. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with terms for the specific areas of interest. Where data were lacking, we relied on opinions of panel members and peer reviewers. STUDY SELECTION AND DATA SYNTHESIS: Studies were reviewed to determine whether patients had heart failure due to systolic dysfunction (left ventricular ejection fraction, < 0.35 to 0.40) and whether clinical outcomes were reported. Studies that reported only intermediate outcomes (eg, hemodynamics) were not reviewed. CONCLUSION: Counseling and education can improve patient outcomes and decrease unnecessary hospitalizations. Patients with mild to moderate heart failure should be restricted to 3 g/d of sodium initially. Those who are unresponsive to this dosage or who have more severe disease should be advised to consume 2 g/d or less. Patients should be strongly advised to drink no more than 30 mL/d of alcohol or, preferably, to abstain completely. Exercise training is safe and can improve exercise duration and symptoms. Adherence to the treatment plan should be stressed and monitored at each visit. Clinicians should inform patients of the seriousness of their disease and their prognosis, but they should emphasize that patients can continue to remain active and enjoy a reasonable quality of life.

Counseling↗
PubMed2006

Effects of cardiac patches engineered with bone marrow-derived mononuclear cells and PGCL scaffolds in a rat myocardial infarction model.

Little is known about the cardioprotective effects against heart failure (HF), the effects on differentiation of bone marrow-derived mononuclear cell (BMMNC), and the biocompatibility of BMMNC-seeded biodegradable poly-glycolide-co-caprolactone (PGCL) scaffolds in a myocardial infarction (MI) animal model. This study hypothesized that implantation of a BMMNC-seeded PGCL scaffold into the epicardial surface in a rat MI model would be biocompatible, induce BMMNC migration into infarcted myocardium, and effectively improve left ventricular (LV) systolic dysfunction. One week after the implantation of a BMMNC-seeded PGCL scaffold, BMMMC showed migration into the epicardial region. Four weeks after implantation, augmented neovascularization was observed in infarcted areas and in infarct border zones. Some BMMNCs exhibited the presence of alpha-MHC and troponin I, markers of differentiation into cardiomyocytes. In echocardiographic examinations, BMMNC-seeded PGCL scaffold and non-cell-seeded simple PGCL scaffold groups effectively reduced progressive LV dilatation and preserved LV systolic function as compared to control rat MI groups. Thus, BMMNC-seeded PGCL scaffolding influences BMMNC migration, differentiation to cardiomyocytes, and induction of neovascularization, ultimately effectively lessening LV remodeling and progressive LV systolic dysfunction. PGCL scaffolding can be considered as an effective treatment alternative in MI-induced advanced HF.

Animals↗
PubMed1986

Asymptomatic severe aortic regurgitation in the young. Hemodynamic and angiographic data in 37 patients with echocardiographic correlation.

The aim of this study was to evaluate from hemodynamic and angiocardiographic (ACG) data the extent of left ventricular (LV) systolic dysfunction in a group of predominantly young (mean age 29 years) asymptomatic patients with severe aortic regurgitation (AR). In addition, echocardiography was performed and these data were correlated with ACG data and the value of these parameters in predicting LV dysfunction was tested. Thirty-seven patients were catheterized and 18 demonstrated LV dysfunction with an ejection fraction (EF) of less than 50%. These patients were classified as group A and the remaining 19 patients with EF greater or equal to 50% formed group B. While there was no difference between the 2 groups with regard to age or regurgitant fraction, the end-diastolic pressure was raised (p less than 0.01) and cardiac index depressed (p less than 0.05) significantly in group A. Of the echocardiographic parameters, the end-systolic diameter (ESD) correlated best with the EF (coefficient of correlation = -0.7 and p less than 0.001). In addition, the ESD was significantly higher in group A (p less than 0.001). When an ESD greater than or equal to 48 mm was used as a predictor of an EF less than 50% (group A) the sensitivity was 89% and the specificity 79%. In conclusion, many young asymptomatic patients with severe AR may have severe LV systolic dysfunction and an ESD greater than or equal to 48 mm is a good predictor of such a subgroup.

Adolescent↗
PubMed2001

Angiotensin-converting enzyme inhibitor dosages in elderly patients with heart failure.

BACKGROUND: We sought to describe the dosages of angiotensin-converting enzyme (ACE) inhibitor prescribed to elderly patients with heart failure at hospital discharge, the factors associated with dosing level, and the association of these dosages with 1-year outcomes. METHODS: Demographic, procedural, and medication data were collected retrospectively from medical records at 18 Connecticut hospitals. Information on mortality and readmission was obtained from the Health Care Financing Administration administrative databases. Dosages of ACE inhibitor were grouped into 3 categories: dosages recommended in practice guidelines or higher (target dose), dosages used in clinical trials but lower than guideline recommendations (subtarget dose), and dosages lower than those used in clinical trials (low dose). RESULTS: A total of 554 patients, 65 years old or less with confirmed heart failure and systolic dysfunction, were prescribed an ACE inhibitor at discharge. Target, subtarget, and low doses were given in 19%, 63%, and 18% of the patients, respectively. Few demographic or clinical factors were related to lower dosages. Both subtarget and target doses of ACE inhibitors were associated with a significantly lower adjusted 1-year mortality (relative risk 0.67, P =.04; relative risk 0.51, P =.02, respectively) compared with low doses of ACE inhibitors. CONCLUSIONS: In a representative elderly cohort of patients with heart failure with systolic dysfunction, the majority (82%) were discharged on doses of ACE inhibitors consistent with those used in clinical trials. We observed a dose-response relationship between higher doses and lower mortality. Future studies will need to determine whether this association is causal.

Aged↗
PubMed2005

Multimodal detection of perioperative myocardial ischemia.

Cardiac anesthesiologists have the responsibility to detect myocardial ischemia in a timely manner, which can be a challenging task in the perioperative environment. Transesophageal echocardiography pulmonary artery catheterization, and electrocardiography are the 3 major methods available for monitoring perioperative ischemia. Echocardiography, the newest and most sophisticated method, has been shown to be highly sensitive for detecting ischemia associated with systolic dysfunction. Echocardiography can detect wall-motion abnormalities before electrocardiographic changes develop in patients who are likely to experience supply-mediated ischemia. Perioperative ischemia that occurs after bypass and is detected using transesophageal echocardiography has been found to be related to an adverse outcome. However, the use of echocardiography has some limitations, including the detection of abnormalities not induced by ischemia and the presence of ischemia in areas not visible in the view selected. Pulmonary artery catheterization can provide information about systolic dysfunction, diastolic dysfunction, and mitral regurgitation, but the sensitivity and safety of catheterization have been questioned. Electrocardiography can be a superb monitoring device as long as clinicians pay adequate attention to lead selection and placement, filter selection, and gain adjustment. The optimal monitoring approach should integrate all 3 available monitoring systems in order to increase the likelihood of detecting both supply- and demand-mediated ischemia.

Anesthesiology↗
PubMed2005

[Predictive factors for readmission in heart failure patients].

BACKGROUND AND OBJECTIVE: Heart failure (HF) is a prevalent and increasing disease and represents one of the main causes of hospital admission. It is associated with an important morbi-mortality and a high rate of readmission. The objective of this study was to know the clinical characteristics of admitted patients with HF and to detect any valuable prognosis factors. PATIENTS AND METHOD: Prospective study of admitted HF patients between May'99 and May'00. Readmission rate was evaluated six months later. RESULTS: 204 patients were included with an average age of 78 (9.9) years. 66% were women. Diabetes mellitus (DM) (36.4%) and chronic obstructive pulmonary disease (COPD) (23.4%) were the most outstanding associated pathologies. Ischemic heart disease (IHD) was the most frequent etiology in 33.4% cases. Mean time of admission was 10 days. 34% patients had systolic dysfunction (SD). Men with IHD presented a higher rate of SD (p < 0.001). Mortality was 12.4%, especially in COPD patients (p < 0.011). IECAs were prescribed in 71.2% in the SD group. Readmission rate at 6 months was about 43%. Patients with renal failure (p < 0.04) and those with a more impaired functional class (p < 0.02) displayed a higher readmission rate. CONCLUSIONS: Several clinical factors determine the morbi-mortality and prognosis including an older age, associated comorbility, type of cardiopathy and presence of systolic dysfunction. All these factors are detected at the time of hospital admission.

Aged↗