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Managed care patients with heart failure: spectrum of ventricular dysfunction and predictors of medication utilization.

BACKGROUND: Heart failure (HF) is a common clinical syndrome resulting in high morbidity and mortality. We examined the spectrum of ventricular dysfunction, and investigated the predictors of angiotensin-converting enzyme (ACE) inhibitor, beta-blocker, and spironolactone prescription in 1613 managed care patients with HF. METHODS AND RESULTS: The diagnosis of HF was made by a HF discharge diagnosis or at least 3 physician encounters with a HF diagnosis during 2000. Logistic regression was used to identify predictors of medication prescription. Preserved systolic function was documented in 37%, moderate-severe systolic dysfunction in 31%, mild systolic in 14%, and 18% had inadequate documentation. The mean age was 69 years, 58% were women, 24% African American, and 60% were Medicare patients. Patients without HF type documented were the least aggressively treated. Coronary artery disease, hypertension, and diabetes predicted increased utilization of ACE inhibitor and beta-blocker therapies. History of nephropathy was associated with less ACE inhibitor prescription. Advancing age predicted less utilization of beta-blockers and spironolactone. Neither ethnicity nor gender influenced medication prescription. CONCLUSION: Preserved left ventricular function was common. Documentation of significant systolic dysfunction was associated with improved quality of care. Interventions to encourage documentation of HF type and further study of HF with preserved systolic function are warranted.

Adrenergic beta-Antagonists↗

[Heart failure due to diastolic dysfunction: the treatment principles].

The clinical relevance of diastolic dysfunction in heart failure has recently been emphasized. In fact, the presence of signs of heart failure does not imply a depressed left ventricular systolic function; moreover, the severity of heart failure and effort tolerance are more closely related to diastolic than to systolic indexes. However, the principal trials about the treatment of heart failure were mainly addressed to patients with significant left ventricular systolic dysfunction, whereas the optimal therapy for diastolic dysfunction is not well known. The aim of this review was to assess the rationale and the therapeutic options in heart failure due to diastolic dysfunction. A diastolic dysfunction can be exclusive or associated with systolic dysfunction, as in dilated cardiomyopathy. It has to be noted that in this disease an improvement of diastolic function was demonstrated for most of the drugs currently employed in the treatment of heart failure, such as vasodilators, ACE inhibitors, beta-blockers, digitalis, and other inotropic drugs. Moreover, the favorable effect of the treatment on diastolic parameters (reduction of left ventricular filling pressure, regression of restrictive filling pattern) is associated with a positive prognostic impact. The main objective of the treatment of heart failure with preserved left ventricular systolic function is to control the symptoms by means of lowering high left ventricular filling pressure without significantly lowering cardiac output. According to the therapeutic guidelines of the American College of Cardiology/American Heart Association Task Force, the drugs indicated to treat symptomatic patients with heart failure and preserved left ventricular systolic function are diuretics and nitrates. Potentially useful, but with insufficiently proven efficacy are beta-blockers, calcium antagonists and ACE inhibitors, whereas direct vasodilators and inotropic drugs were considered inadvisable. It is important to remember that the treatment might possibly be oriented to the cause and also to the possible precipitating factors of the heart failure syndrome (i.e. ischemia, tachycardia, arrhythmias, hypertension). In conclusion, considering the relatively common incidence of heart failure due to prevalent diastolic dysfunction, and the few available data about the therapeutic options in these patients, large multicenter trials devoted to the treatment of this syndrome are needed.

Cardiovascular Agents↗

Assessment of acute right ventricular dysfunction induced by right coronary artery occlusion using echocardiographic atrioventricular plane displacement.

Right ventricular (RV) systolic function analysis by echocardiography has traditionally required RV endocardial border definition with subsequent tracing and is often inaccurate or impossible in technically poor studies. The atrioventricular plane displacement (AVPD) method attempts to use the descent of the tricuspid annular ring, a reflection of the longitudinal shortening of the right ventricle, as a surrogate marker for RV systolic function. We hypothesized that RV ischemia induced during right coronary artery occlusion proximal to the major right ventricular branches would result in severe right ventricular systolic dysfunction detectable by the AVPD method. During this pilot study, seven patients undergoing elective proximal RCA angioplasty had echocardiographic measurement of RV AVPD performed at baseline (i.e., immediately prior to RCA balloon inflation), during the last 30 seconds of first RCA balloon inflation, and at 1 minute after balloon deflation (recovery). Lateral and medial RV AVPD were significantly reduced from baseline values during intracoronary balloon inflation. (Lateral: 2.45 cm +/- 0.22 vs 1.77 cm +/- 0.13, P < 0.001; medial: 1.46 cm +/- 0.37 vs 1.28 cm +/- 0.32, P < 0.05). Additionally, lateral and medial RV AVPD significantly returned towards baseline values during recovery. (Lateral: 2.39 cm +/- 0.20, P < 0.001; medial: 1.58 cm +/- 0.27, P = 0.01). At baseline, all lateral RV AVPD values were > 2.0 cm, whereas during balloon inflation all were < 2.0 cm. No such clear distinction was found in medial RV AVPD values. Proximal RCA angioplasty is associated with a significant reduction in lateral and medial RV AVPD. Thus RV AVPD may serve as a marker for RV systolic dysfunction.

Acute Disease↗

[Cardiac failure in ischemic cardiopathy].

Heart failure is a major cause of morbidity and mortality and represents an important recognized health problem. Heart (or cardiac) failure is the pathophysiological state in which a myocardial dysfunction is frequently but non always responsible for the inability of the heart to pump blood at a rate commensurate with tissues metabolic requirements. Ischemic heart disease is the commonest cause of heart failure frequently associated with left ventricular systolic dysfunction, although some patients, particularly the elderly, have diastolic dysfunction. Coronary heart disease is responsible for left ventricular systolic dysfunction (and cardiac failure) in the acute and chronic stage. Myocardial dysfunction is usually a consequence of myocardial infarction that may lead to ventricular remodeling with compensatory dilation and hypertrophy and subsequent systolic and diastolic dysfunction resulting in heart failure. Many patients with heart failure and/or left ventricular dysfunction are unknown. The echocardiographic screening of patients with known or suspected left ventricular dysfunction remains an important topic for future clinical epidemiological research and allows for improvement of therapeutic management of patients with cardiac dysfunction.

Echocardiography↗

[Heart failure in internal medicine departments].

BACKGROUND: The profile of patients with heart failure varies according to the healthcare setting and specialty. A national survey was carried out by the Working Group on Heart Failure of the Spanish Society of Internal Medicine in order to define the profile of patients with heart failure hospitalized in Spanish Internal Medicine Departments. PATIENTS AND METHOD: National registry including 51 hospitals all over Spain and 2145 patients suffering from this pathology. RESULTS: Patients' median age was 77.2 years, 57.3% women and 42.7% men. There was a high percentage of illiteracy and low cultural level among patients (58.9%). In addition, many patients were found to have impaired physical and/or cognitive functions (67.4%). There was also a high incidence of related illnesses. Hypertension was the most frequent cause of heart failure. Echocardiography was performed in less than a quarter of patients and left ventricular ejection fraction was greater than 45% in more than a half (53.7%). At discharge, diuretics were the mostly prescribed drugs (92.5%). Angiotensin-converting enzyme inhibitors were prescribed in 66.1% patients (73.4% in patients with known systolic dysfunction) and beta-blockers in 9.8% (12.3% in patients with known systolic dysfunction). CONCLUSIONS: In Spain, patients hospitalized for heart failure in Internal Medicine Departments use to be elderly women with preserved left ventricular systolic function, low cultural level and physically handicapped. This profile is pretty different from that reported in published clinical trials.Therefore, we should consider the most appropriate management of these patients with regard to treatment, hospitalization and follow-up.

Adult↗

Assessment of systolic and diastolic LV function by MR myocardial tagging.

Heart failure has been divided into several different forms depending on etiology, clinical course and pathophysiology of left ventricular (LV) dysfunction. Systolic and diastolic dysfunction are characterized by a reduced cardiac output with normal (= diastolic dysfunction) or depressed (= systolic dysfunction) LV pump function. New diagnostic techniques such as magnetic resonance imaging (MRI) allow to determine noninvasively LV 3D motion by labelling specific myocardial regions (= myocardial "tagging") with a rectangular or radial grid. From the deformation of this grid rotational and translational motion of the heart can be derived. A "wringing" motion of the left ventricle has been described during systole which includes a clockwise rotation at the base and a counterclockwise rotation at the apex. During diastole, an "untwisting" motion has been demonstrated. In the normal heart, diastolic "untwisting" occurs primarily during isovolumic relaxation, analogous to the systolic "wringing" which takes place mainly during isovolumic contraction. A prolongation of the "untwisting" motion was found in the hypertrophied (aortic stenosis) and hibernating myocardium. Thus, heart failure is associated with profound alterations in the mechanical function of the heart which are manifested by changes in systolic "wringing" and diastolic "untwisting" motion.

Animals↗

Does load-induced ventricular hypertrophy progress to systolic heart failure?

Ventricular hypertrophy develops in response to numerous forms of cardiac stress, including pressure or volume overload, loss of contractile mass from prior infarction, neuroendocrine activation, and mutations in genes encoding sarcomeric proteins. Hypertrophic growth is believed to have a compensatory role that diminishes wall stress and oxygen consumption, but Framingham and other studies established ventricular hypertrophy as a marker for increased risk of developing chronic heart failure, suggesting that hypertrophy may have maladaptive features. However, the relative contribution of comorbid disease to hypertrophy-associated systolic failure is unknown. For instance, coronary artery disease is induced by many of the same risk factors that cause hypertrophy and can itself lead to systolic dysfunction. It is uncertain, therefore, whether ventricular hypertrophy commonly progresses to systolic dysfunction without the contribution of intervening ischemia or infarction. In this review, we summarize findings from epidemiologic studies, preclinical experiments in animals, and clinical trials to lay out what is known-and not known-about this important question.

Animals↗

Aldosterone Receptor Blockers in the Treatment of Heart Failure.

Heart failure is associated with neurohormonal activation, including activation of the renin-angiotensin-aldosterone system. Plasma aldosterone levels are elevated in patients with heart failure in spite of the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers because of angiotensin-independent stimuli for aldosterone production. In addition to its long recognized role in sodium retention, aldosterone has a number of other deleterious effects, including the increase in myocardial and vascular fibrosis and myocardial remodeling in patients with heart failure. Based on strong clinical trial data, low-dose aldosterone receptor blockers are recommended to improve morbidity and mortality in patients with severe chronic heart failure due to left ventricular systolic dysfunction and in patients with heart failure associated with left ventricular systolic dysfunction after acute myocardial infarction, and in patients already on standard therapy including ACE inhibitors (or angiotensin receptor blockers) and beta blockers. In view of the potential for serious hyperkalemia with the use of aldosterone receptor blockers, it is essential to monitor serum potassium closely and to adjust the dose of aldosterone antagonists based on serum potassium levels. Close adherence to the dosing regimens used in the clinical trials (RALES and EPHESUS ) is recommended. These agents should not be initiated in patients with severe renal insufficiency and closer monitoring is warranted in those with mild to moderate renal insufficiency or diabetes.

Journal Article↗

Advanced hypertensive heart disease in spontaneously hypertensive rats. Lisinopril-mediated regression of myocardial fibrosis.

Left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR) is accompanied by a structural remodeling of the myocardium that includes myocyte hypertrophy and interstitial and perivascular fibrosis of intramyocardial coronary arteries. The structural abnormalities related to fibrous tissue accumulation lead to increased myocardial diastolic stiffness and ultimately impaired systolic function of the left ventricle. It has been shown in 14-week-old SHR with early hypertensive heart disease that myocardial fibrosis could be reversed and myocardial diastolic stiffness normalized by 12-week treatment with the angiotensin-converting enzyme inhibitor lisinopril. Whether such functional defects of the myocardium, based on adverse structural changes, are also reversible in advanced hypertensive heart disease has been questioned. Therefore, we treated 78-week-old male SHR that had chronic hypertension and advanced LVH with severe myocardial fibrosis and age- and sex-matched normotensive Wistar-Kyoto rats (WKY) with 20 mg/kg per day oral lisinopril for 8 months. Compared with untreated SHR or WKY, we found the following: (1) Systolic arterial pressure was normalized (P < .025) and LVH completely reversed (P < .025) in SHR, with no significant reduction in systolic arterial pressure or left ventricular mass in WKY; (2) morphometrically determined myocardial fibrosis in SHR was significantly reversed (P < .025) and associated with improved diastolic stiffness (P < .05), which was measured in the isolated heart by calculation of the stiffness constant of the myocardium; no significant changes occurred in WKY; (3) reversal of myocardial fibrosis was accompanied by an increase (P < .025) in myocardial matrix metalloproteinase 1 activity determined by degradation of [14C]collagen with myocardial tissue extracts after trypsin activation of myocardial promatrix metalloproteinase 1; matrix metalloproteinase 1 activity remained unchanged in WKY treated with lisinopril; and (4) systolic dysfunction, measured by a significantly (P < .025) diminished slope of the systolic stress-strain relation under isovolumic conditions of the left ventricle, was found in 110-week-old SHR, and it could be prevented by lisinopril treatment. Thus, long-term angiotensin-converting enzyme inhibition with lisinopril normalized arterial pressure and LVH, reversed myocardial fibrosis, and improved abnormal myocardial diastolic stiffness in advanced hypertensive heart disease in SHR. In addition, systolic dysfunction of the left ventricle could be prevented. The fibrolytic response to lisinopril was at least partly due to enhanced collagen degradation by activation of tissue matrix metalloproteinase 1.

Angiotensin-Converting Enzyme Inhibitors↗

Treatment of acute myeloid leukemia during the second and third trimesters of pregnancy.

Fortunately, the occurrence of acute myeloid leukemia (AML) during pregnancy is rare. We report a case of successful fetal outcome with standard induction and consolidation treatment in the second and third trimesters, respectively. A 37-year-old woman in her second trimester (21 wks) of pregnancy was found to have acute myeloid leukemia. She elected to maintain the pregnancy and underwent induction with cytarabine and idarubicin. Her hospital course was complicated by Pseudomonas vesicularis and gram-positive bacilli (not Bacillus anthracis) septicemia, but she obtained complete remission. After discharge, a fetal echocardiogram at 26 weeks revealed a mildly dilated right ventricle with mild systolic dysfunction, and the left ventricle appeared smaller than normal with mild systolic dysfunction. The patient then received consolidation therapy with high-dose cytarabine. On day 14 of consolidation, filgrastim 16 mug/kg was added to improve stem cell mobilization. A total of 19.8x10(6) CD34+ cells/kg were collected with a single apheresis session. At 37 weeks, she delivered a viable female infant weighing 3 lbs 12 oz. Fetal abnormalities included acrocyanosis, shallow sacral dimple, short digits and limbs, and prominent frontal skull with mild macrognathia. A postnatal echocardiogram revealed a moderate-sized membranous ventricular septal defect. The ventricular septal defect proved significant and required surgical repair at 5 months. Approximately 4 weeks after delivery, the mother underwent autologous peripheral stem cell transplantation. Unfortunately, 100 days after transplantation, she had a relapse of AML. After a brief remission from a second induction, the patient died.

Adult↗

[Congestive heart failure in the aged. Diagnosis].

THREE DIAGNOSTIC PITFALLS: The difficulty in diagnosing congestive heart failure in the elderly subject is basically caused by three factors. First, clinical expression is often atypical. Secondly, severity is often underestimated as the prevalence of asymptomatic systolic dysfunction increases with age. Half of all cases of left ventricular systolic dysfunction go unrecognized if clinical signs alone are considered. Finally, the pathophysiology of diastolic dysfunction, which predominates in the over 75 population, is still poorly understood. COMPLEMENTARY EXPLORATIONS: As the clinical signs are the same whatever the mechanism of the ventricular dysfunction, echocardiography is the key exploration for diagnosis and for guiding management. Comorbidity is often a confounding factor preventing precise diagnosis and risk stratification.

Aged↗

[Heart failure caused by severe systolic ventricular dysfunction of hypertensive origin. Long-term clinical and functional course].

AIMS: The aims of our study were to evaluate survival and evolution of functional class and ventricular function in patients with severe congestive heart failure due to dilated cardiomyopathy. METHODS: Inclusion criteria were: class III or IV heart failure, dilated left ventricle with ejection fraction < 40%, history of poor controlled hypertension, and exclusion of other etiologies for heart failure. We studied 17 patients with these features; mean age was 64 +/- 7 years and 70% were male. They were followed up during a mean period of 3.3 +/- 1 years (2 to 6; median 3 years). RESULTS: Baseline left ventricular ejection fraction was 30 +/- 5% (20 to 40); 35% of patients were in functional class III and 65% in class IV; 100% of patients received ACE inhibitors and diuretics, 53% betablockers, and 35% calcium-antagonists. Survival was 100%. Left ventricular ejection fraction increased from 30 +/- 5% to 44 +/- 11% at one year, to 50 +/- 11% at 3 years and 51 +/- 10% at the end of follow-up (p < 0.001). This improvement was mainly due to a reduction in systolic left ventricular diameter (from 51 +/- 4 mm to 42 +/- 11 mm, p < 0.01), since diastolic diameter did not significantly changed (63 +/- 4 to 59 +/- 11 mm). CONCLUSIONS: The evolution of severe systolic left ventricular dysfunction due to arterial hypertension is favourable at long-term, with null mortality and clinical ejection fraction and functional improvement. Nevertheless, the persistence of left ventricular dilatation suggests that myocardial damage caused by chronic pressure overload does not disappear.

Aged↗

Prediction of mean pulmonary wedge pressure using doppler pulmonary venous flow variables in hypertrophic cardiomyopathy.

We examined whether pulmonary venous flow variables, assessed by transthoracic Doppler echocardiography, could predict mean pulmonary wedge pressure in hypertrophic cardiomyopathy. Forty-four patients with no left ventricular systolic dysfunction (left ventricular fractional shortening > or =25%) were studied. Forty patients with systolic dysfunction (dilated cardiomyopathy group) served as control. Mitral and pulmonary venous flow velocity curves were recorded with the pulsed-Doppler method and were related to mean pulmonary wedge pressure obtained by right heart catheterization. In hypertrophic cardiomyopathy group, the systolic (r=-0.15, P=0.335) and diastolic (r=0.35, P=0.022) forward flow velocity were poorly related to mean pulmonary wedge pressure, whereas the velocity of atrial reversal (r=0.68, P<0.001) correlated well with mean pulmonary wedge pressure. In dilated cardiomyopathy group, the systolic (r=-0.51, P=0.001) and diastolic (r=0.60, P<0.001) forward flow velocity were strongly related to mean pulmonary wedge pressure. With the cut-off value set at the velocity of atrial reversal >30 cm/s in hypertrophic cardiomyopathy group, the sensitivity for predicting mean pulmonary wedge pressure >15 mmHg was 79% and the specificity was 73%. In conclusion, the atrial component of the pulmonary venous flow can be used to predict mean pulmonary wedge pressure in hypertrophic cardiomyopathy.

Adult↗

Congestive heart failure due to hypertensive ventricular diastolic dysfunction.

Left ventricular (LV) diastolic dysfunction is the first discernible manifestation of heart disease in hypertensive patients. Arterial hypertension with LV hypertrophy leads to reduced preload followed by impaired cardiac output (systolic dysfunction stemming from primary diastolic dysfunction). Diastolic dysfunction leads more often than systolic dysfunction to hypertensive heart failure and is in many cases clearly distinguishable from heart failure with low ejection fraction (EF). Mortality due to heart failure from impaired inotropism is higher than mortality due to diastolic dysfunction, but morbidity is lower. Hypertensive cardiomyopathies can be divided into 4 ascending categories, according to the pathophysiologic and clinical impact of hypertension on the heart: Degree I: LV diastolic dysfunction with no associated LV hypertrophy Degree II: LV diastolic dysfunction with echocardiographic LV hypertrophy Degree IIA: Normal exercise capacity in terms of maximal oxygen consumption Degree IIB: Impaired exercise capacity in terms of maximal oxygen consumption Degree III: Congestive heart failure (severe dyspnea and radiographically determined pulmonary edema with normal (> or = 50%) EF Degree IIIA: LV mass/volume ratio > 1.8 with little or no myocardial ischemia Degree IIIB: LV mass/volume ratio < 1.8 with significant myocardial ischemia Degree IV: Profile of dilated cardiomyopathy; LV hypertrophy and impaired EF (< 50%).

Cardiac Output↗

Determination of left ventricular filling pressure by Doppler echocardiography in patients with coronary artery disease: critical role of left ventricular systolic function.

OBJECTIVES: This study was designed to determine the usefulness of transthoracic Doppler measurements in detecting increased left ventricular (LV) end-diastolic pressure in patients with coronary artery disease, specifically examining the influence of systolic function on the accuracy of these methods. BACKGROUND: Studies that have correlated Doppler indexes with LV filling pressures primarily involved patients with LV systolic dysfunction. The reliability of Doppler indexes in estimating filling pressures in patients with coronary artery disease and preserved systolic function is unclear. METHODS: Pulsed wave Doppler transmitral and pulmonary venous flow velocity curves and LV pressure were recorded in 83 patients with coronary artery disease. RESULTS: Conventional Doppler indexes (deceleration time of mitral E wave velocity, ratio of peak mitral E to A wave velocities and pulmonary venous systolic fraction) correlated with LV filling pressure in patients with an ejection fraction (EF) < or = 50% but not in those with an EF > 50%. Previously published regression analysis for prediction of LV filling pressure was accurate in patients with an EF < or = 50% but not in those with an EF > 50%. The difference between flow duration with atrial contraction in the pulmonary veins and transmitral flow duration with atrial contraction correlated with LV filling pressure in both groups. CONCLUSIONS: Analysis of the early diastolic portion of the transmitral or pulmonary venous flow velocity curves can be used to predict LV filling pressures in patients with systolic dysfunction, but are inaccurate in patients with preserved systolic function. The combined analysis of both flow velocity curves at atrial contraction is a reliable, feasible predictor of increased LV filling pressure, irrespective of systolic function.

Aged↗

[Left ventricular dysfunction induced by monomorphic ventricular arrhythmias: large improvement in ventricular function after radiofrequency ablation of the arrhythmic source].

Left ventricular systolic dysfunction related to ventricular arrhythmias is a relatively poorly understood entity. To increase our knowledge base, we describe 5 patients in whom the link between ventricular dysfunction and ventricular arrhythmia was unequivocally established. All patients had repetitive monomorphic ventricular arrhythmias and left ventricular systolic dysfunction (ejection fraction < or =40% and end-diastolic size > or =55 mm). The arrhythmogenic source was identified by electrophysiological study (right ventricle in 2 patients, left ventricle in 2, and left sinus of Valsalva in one), and was eliminated in all patients by radiofrequency catheter ablation. At 7+/-2 months post-ablation, large improvements were seen in left ventricular function and remodeling (ejection fraction >/=50% and end-diastolic size < or =51 mm in all cases), with no recurrence of arrhythmia during follow-up (10-69 months). This finding confirms that recurring ventricular arrhythmias can induce left ventricular dysfunction which may be reversible after ablation.

Adult↗

Combined right ventricular systolic and diastolic dysfunction represents a strong determinant of poor prognosis in patients with symptomatic heart failure.

BACKGROUND: The presence of right ventricular systolic dysfunction is known to significantly worsen prognosis of patients with heart failure. However, the prognostic impact of right ventricular diastolic dysfunction and of its combination with right ventricular systolic dysfunction and with other prognostic markers has not yet been systematically studied. The aim of this study was to assess the prognostic impact of combined right ventricular systolic and diastolic dysfunction in patients with symptomatic heart failure due to ischemic or idiopathic dilated cardiomyopathy. METHODS: The study included 177 consecutive patients with symptomatic heart failure (mean left ventricular ejection fraction of 23%). All patients underwent clinical and laboratory examination, standard echocardiography completed by Doppler tissue imaging of the tricuspid annular motion, and right-sided heart catheterization. They were followed up for a mean period of 16 months (range, 1-48 months). RESULTS: During the follow-up, there were 28 cardiac-related deaths and 35 non-fatal cardiac events (31 hospitalizations for heart failure decompensation and 4 hospitalizations for malignant arrhythmias requiring the implantation of a cardioverter-defibrillator). The multivariate stepwise Cox regression modeling revealed the right ventricular systolic (represented by the peak systolic tricuspid annular velocity-Sa) and diastolic (represented by the peak early diastolic tricuspid annular velocity-Ea) function to be the independent predictors of event-free survival or survival (p<0.01). The Sa separated better between patients with and without the risk of cardiac events (p<0.05), while the Ea appeared to further distinguish patients with increased risk (those at risk of late event from those at risk of early non-fatal event and early death). The strongest predictive information was obtained by the combination of Sa and Ea creating the Sa/Ea categories. The Sa/Ea I category of patients (Sa>or=10.8 cm s(-1) and Ea>or=8.9 cm s(-1)) had excellent prognosis. On the other hand, the Sa/Ea IV category (Sa<10.8 cm s(-1) and Ea<8.9 cm s(-1)) was found to be at a very high risk of cardiac events (p<0.001 vs. Sa/Ea I). Imbalanced categories of patients (Sa/Ea II and III) with only one component (Sa or Ea) pathologically decreased were at medium risk when assessing event-free survival. However, a significantly better survival (p<0.05) was found in patients with Ea>or=8.9 cm s(-1) (Sa/Ea I and III categories) as compared with those having Ea<8.9 cm s(-1) (Sa/Ea II and IV categories). Thus, in contrast to event-free survival, the survival pattern was determined mainly by the Ea value with only little additional contribution of Sa. CONCLUSIONS: The assessment of right ventricular systolic and diastolic function provides complementary information with a very high power to stratify prognosis of patients with heart failure. The combination of right ventricular systolic and diastolic dysfunction identifies those with a very poor prognosis.

Blood Flow Velocity↗

Unrecognized myocardial infarction: the association with cardiopulmonary symptoms and mortality is mediated via echocardiographic abnormalities of global dysfunction instead of regional dysfunction: the Olmsted County Heart Function Study.

BACKGROUND: There are very few data describing the association of electrocardiogram-based unrecognized myocardial infarction (ECG-UMI) with nonanginal cardiopulmonary symptoms, echocardiographic abnormalities, and mortality in the community. METHODS: We studied 2042 Olmsted County residents, who were randomly selected and aged > or = 45 years, by a survey questionnaire for symptoms, echocardiogram for structural abnormalities, and a 5-year follow-up for all-cause mortality. Unrecognized myocardial infarctions (n = 81) were diagnosed if ECG-based myocardial infarction (MI) criteria were met without the history of a documented recognized MI. RESULTS: In UMI versus no MI controls, the prevalence (%) of dyspnea on exertion (49 vs 29), orthopnea (6 vs 4), palpitations (20 vs 15), and history of fluid overload (6 vs 1) was significantly higher (P < .05). The associations of exertional dyspnea and history of fluid overload with UMI were independent of age, sex, and pulmonary disease but had a significant reduction in their magnitude after adjusting for global dysfunction (diastolic or systolic dysfunction). All the 4 symptoms were associated with increased risk of mortality (hazard ratios ranging from 2.3 to 9.1, P < .0001), which was meaningfully attenuated by adjusting for ECG-UMI status. Global ventricular dysfunction had a more significant impact on this association than regional ventricular dysfunction (wall motion abnormalities). CONCLUSIONS: The increased risk of mortality associated with symptoms is at least in part mediated via ECG-UMI. Structural abnormalities of global dysfunction play a greater role in mediating this risk than regional dysfunction, challenging the current clinical practice of calling an ECG-based MI false positive in symptomatic adults in the absence of wall motion abnormalities.

Aged↗