Value of peri-procedural lung ultrasound in predicting heart failure or left ventricular systolic dysfunction within 3 months in STEMI patients undergoing primary PCI

Early Identification of Asymptomatic Subjects at Increased Risk of Heart Failure and Cardiovascular Events: Progress and Future Directions

Section 5: Management of Asymptomatic Patients with Reduced Left Ventricular Ejection Fraction

Left Ventricular Dysfunction and Sleep Apnea Syndrome: Cause or Consequence?

Heart failure is one of the most common conditions of industrialized society and at its most florid encompasses a constellation of symptoms and signs associated with demonstrable left ventricular systolic dysfunction (LVSD) [1]. Many patients with clinical symptoms and signs of heart failure have no apparent abnormality of ventricular contractile function but may have diastolic heart failure; in addition many patients with left ventricular systolic or diastolic dysfunction do not have any symptoms of heart failure. For the purposes of this review, LVSD refers to demonstrable left ventricular systolic dysfunction, and heart failure to symptomatic left ventricular dysfunction. Since heart failure is often asymptomatic and for other reasons the diagnosis of heart failure is often difficult. As a result many patients with the condition, in particular when asymptomatic, are denied appropriate pharmacological intervention. The ability to diagnose heart failure from a blood test would not have been predicted even a few years ago. However our increased understanding of heart failure as a complex clinical syndrome associated with marked neurohormonal activation has led to the search for a simple, diagnostic blood-test for the condition. That search may now be coming to fruition with the natriuretic peptides showing the most promise. The primary aetiological factors in industrialized countries are ischaemic heart disease, hypertension and diabetes, either singly or in combination [2]. Approximately 85% of cases of heart failure in the general population are associated with either coronary disease or hypertension [3]. The clinical syndrome has an estimated prevalence of approximately 1% of the population as a whole and perhaps as high as 10% of those greater than 75 years old [4]. Many patients with significant myocardial damage pass through a period of asymptomatic left ventricular dysfunction before developing overt symptoms, i.e. clinical heart failure. Indeed at any one time there are at least as many individuals with asymptomatic (and largely undiagnosed) LVSD as there are patients with clinical heart failure; the prevalence of asymptomatic LVSD in a recent population based echocardiographic study was around 3% [5]. Clearly, the apparent incidence and prevalence of LVSD and asymptomatic heart failure depend upon definitions of the terms ‘LVSD’ and ‘symptoms’. However in the study of McDonagh et al. [5], LVSD was defined as an echocardiographic ejection fraction of ≤ 30%, a strict definition which excluded many patients who in day to day clinical practice would be considered to have LVSD (i.e. ejection fraction 30–40%). A combination of factors explains the increasing incidence and prevalence of heart failure: improvements in survival following acute myocardial infarction, in the treatment of hypertension, and in secondary prevention following such events coupled with an increasing number of elderly individuals within the population. Increasing awareness of the problem may also be a contributory factor. It should be emphasized at this point that a diagnosis of heart failure carries with it a very poor prognosis, with mortality similar to that for the common malignant diseases. Even in the current era of vasodilator therapy for the treatment of heart failure, approximately 65% of subjects will die within 5 years of diagnosis [6]. In addition, the potential impact upon quality of life should not be understated. A number of studies of common illnesses have indicated that quality of life for patients with heart failure is worse than that in arthritis, diabetes or chronic obstructive pulmonary disease [7, 8]. In addition heart failure represents one of the major reasons for emergency hospital admission [9]. Therefore it is not surprising that heart failure is a major economic burden to the health care systems of developed countries, accounting for 1–2% of total health care expenditure, 70% of which is related to hospitalization [10]. Although there are clearly major implications incumbent on health services provision, there has been a relative neglect of the problem of heart failure by those responsible for the provision of services, a point illustrated by the absence of mention of heart failure in the Government's Health of the Nation report published in 1991 [11].

The prevalence of treatable left ventricular systolic dysfunction in patients who present with noncardiac vascular episodes: A case-control study

Section 7: Heart Failure in Patients With Left Ventricular Systolic Dysfunction

Risk Factors for Acute Renal Insufficiency Induced by Diuretics in Patients With Congestive Heart Failure

The patient, W.L., is a 62-year-old white man with a history of hypertension, hypercholesterolemia, and an anterior Q-wave myocardial infarction 3 years ago. He has had 2 admissions for heart failure in the past 6 months. He was last discharged 2 months ago on aspirin 325 mg daily, simvastatin 40 mg daily, enalapril 10 mg BID, metoprolol XL 100 mg daily, digoxin 0.25 mg daily, and furosemide 120 mg BID. Over the past month, he has noted some increasing dyspnea on exertion and occasional episodes of paroxysmal nocturnal dyspnea but has not had any increase in peripheral edema or body weight. His left ventricular ejection fraction on discharge from the hospital 2 months ago was 26%, with evidence of a large anterior akinetic area but without evidence of inducible myocardial ischemia on dobutamine echocardiography. His laboratory data today included a hematocrit of 41%, serum creatinine 1.1 mg%, potassium 4.1 meq/L, fasting blood sugar 108 mg%, LDL cholesterol 92 mg/dL, HDL cholesterol 45 mg/dL, triglycerides 188 mg/dL, serum digoxin level 1.2, and brain natriuretic peptide (BNP) (Biosite) 508. ECG revealed evidence of an old anterior myocardial infarction, and chest x-ray showed cardiomegaly with some increase in pulmonary vascularity. At this time, would you suggest any change in his medical regimen? Angiotensin-converting enzyme (ACE) inhibition and β-blockade have been shown effective in improving survival in patients with systolic left ventricular dysfunction (SLVD) resulting from both ischemic and nonischemic cardiomyopathy; they are indicated in all patients with heart failure (HF) caused by SLVD unless contraindicated or not tolerated. Although they improve the symptoms of HF, loop diuretics and digoxin have not been shown to reduce mortality rate. There is, however, increasing evidence that aldosterone blockade is effective in reducing mortality and morbidity rates in patients with HF caused by SLVD that is associated …

Major uncertainty remains about the relationship between left ventricular (LV) systolic dysfunction, recurrent stroke, and the optimal antithrombotic therapy for secondary stroke prevention in patients with recent stroke and LV systolic dysfunction. We performed a post hoc analysis of data from the ARCADIA trial (Atrial Cardiopathy and Antithrombotic Drugs in Prevention After Cryptogenic Stroke), a randomized trial comparing apixaban versus aspirin for secondary stroke prevention in patients with cryptogenic stroke and atrial cardiopathy. Echocardiograms were sent from 185 enrolling sites in the United States and Canada for central review at the trial echocardiography laboratory. We defined LV systolic dysfunction as LV fractional shortening <25%, LV ejection fraction <50%, or any LV wall motion abnormality. The primary outcome of interest was recurrent ischemic stroke. First, we built Cox proportional hazard models to evaluate the association between LV systolic dysfunction and recurrent ischemic stroke risk adjusted for imbalanced covariates. Next, we used Cox proportional hazard models and interaction terms to compare the effect of apixaban versus aspirin on the outcome of interest in patients with and without LV systolic dysfunction. Among 964 patients with complete echocardiographic data of the 1015 patients enrolled in the trial, 165 (17.1%) had LV systolic dysfunction (mean age, 67 years; 43% female; mean follow-up, 1.7 years), and 799 (82.9%) had no LV systolic dysfunction (mean age, 68 years; 56% female; mean follow-up, 1.5 years). Recurrent ischemic stroke occurred more frequently in patients with LV systolic dysfunction (n=15, 9.1%) compared with those without LV systolic dysfunction (n=50, 6.3%), but LV systolic dysfunction was not significantly associated with recurrent stroke after adjustment for imbalanced covariates (hazard ratio, 1.3 [95% CI, 0.7-2.4]). Compared with aspirin, apixaban was associated with a significantly reduced risk of recurrent ischemic stroke in patients with LV systolic dysfunction (hazard ratio, 0.24 [95% CI, 0.07-0.87]) but not in those without LV systolic dysfunction (hazard ratio, 1.13 [95% CI, 0.65-1.96]; Pinteraction=0.028). In a secondary analysis of the ARCADIA trial data, apixaban was associated with a significantly lower risk of recurrent ischemic stroke than aspirin in patients with LV systolic dysfunction.

Previous studies have found that plasma B-type natriuretic peptide (BNP) is elevated during left ventricular systolic or diastolic dysfunction. It is unclear whether the ventricular systolic and diastolic function is associated with different levels of plasma BNP. Plasma BNP was measured in 149 heart failure patients by a rapid point-of-care assay. The patients were divided into left ventricular diastolic dysfunction (n = 48), left ventricular systolic dysfunction (n = 62) and right ventricular systolic dysfunction group (n = 39). The mean BNP level in the left ventricular diastolic dysfunction, left ventricular systolic dysfunction and right ventricular systolic dysfunction was 115 +/- 80 pg/ml, 516 +/- 445 pg/ml and 345 +/- 184 pg/ml, respectively (p < 0.05). We concluded that ventricular systolic and diastolic dysfunction increases plasma BNP levels to a different extent. Left and right ventricular systolic dysfunction is associated with a higher level of plasma BNP than left ventricular diastolic dysfunction.

Effectiveness of Echocardiographic Imaging by Nurses to Identify Left Ventricular Systolic Dysfunction in High-Risk Patients

Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease

Introduction: Dialysis patients tend to have a greater prevalence of cardiovascular diseases. Objectives: The aim of this study was to determine the prevalence of heart valve calcification, left ventricular hypertrophy, and left ventricular systolic and diastolic dysfunction. It also aimed to determining the relationship of the above mentioned parameters with serum calcium, phosphorus, parathormon and duration of dialysis. Patients and Methods: This cross-sectional study was conducted on 100 hemodialysis patients who were referred to Hajar hospital in Shahrekord, Iran. Using echocardiography, patients were examined for the calcification of the heart valves, left ventricular hypertrophy, and left ventricular systolic and diastolic dysfunction. Serum calcium, phosphorus, and parathormon and duration of dialysis was also determined. Results: The mean age of the patients was 58.10 ± 15.51 years. Around 24 patients suffered from calcification of the heart valves. Additionally, 85 patients suffered from left ventricular hypertrophy. The prevalence of left ventricular systolic and diastolic dysfunction was 26% and 86%, respectively. Common valvular abnormalities were mitral valve regurgitation (97%), followed by tricuspid regurgitation and aorta-pulmonary disorder, respectively. There was a significant relationship between serum phosphate and calcification of cardiac valves, left ventricular hypertrophy, and left ventricular systolic dysfunction (P 0.05). Conclusion: Cardiovascular diseases are common among hemodialysis patients. Hyperphosphatemia is a risk factor for the prevalence of left ventricular hypertrophy, left ventricular systolic dysfunction and calcification of the heart valves.

This research primarily analyzes the clinical application of two-dimensional speckle tracking imaging (2D-STI), real-time 3-dimensional echocardiography (RT-3DE), and tissue Doppler imaging (TDI) in evaluating left ventricular dysfunction associated with breast cancer (BC) chemotherapy-related cardiotoxicity. First, we selected 106 BC patients who received treatment in The Affiliated Hospital of Chengde Medical University as the research group, all of whom underwent anthracycline-based chemotherapy; another 100 healthy subjects were chosen as the control group. Conventional ultrasound was employed to detect the mitral annular plane systolic excursion (MAPSE), mitral valve orifice early diastolic blood flow velocity (E), and left atrial volume index (LAVI) in the study subjects. 2D-STI was utilized to measure the global longitudinal strain (GLS) of the left ventricle, RT-3DE to measure left ventricular ejection fraction (LVEF), and TDI to measure the ratio of E to the average early diastolic mitral annulus velocity (E/e'), as well as systolic and early diastolic tissue velocities at the lateral wall of the mitral annulus and the ventricular septum (lateral s', septal s', lateral e', and septal e'). Left ventricular dysfunction was analyzed in both groups, and potential influencing factors were discussed. The data revealed markedly lower GLS, MAPSE, E, lateral e', and septal e' in the research group compared to the control group. GLS<15.02% and LVEF<53% were defined as left ventricular systolic dysfunction. In comparison with the control group, the GLS and LVEF abnormality rates were evidently higher in the research group. No left ventricular diastolic dysfunction was observed in patients in both groups. Additionally, the dose of anthracyclines was a potential influencing factor for left ventricular dysfunction. 2D-STI and TDI have certain predictive implications for the occurrence of subclinical left ventricular systolic and diastolic dysfunctions after BC chemotherapy. Furthermore, high-dose anthracyclines might lead to left ventricular dysfunction.

Background and Objectives：About 25% of the patients with non-ischemic left ventricular (LV) systolic dysfunction will improve spontaneously. However, little has been known about the fate of the patients stricken with heart failure after recovery from LV dysfunction. We hypothesized that the patients who recovered from nonischemic LV dysfunction have a substantial risk for recurrent heart failure. Subjects and Methods：Fifty patients (32 males, mean age: 54.9±12.4 years) who recovered from systolic heart failure (LV ejection fraction; an EF of 28.8±7.2% at the initial presentation) to near-normal (LVEF >40% and a 10% or more increase in the absolute value) were monitored for the recurrence of heart failure. Patients with significant coronary artery disease were excluded. The etiologies of heart failure were idiopathic dilated cardiomyopathy (n=39), alcoholic cardiomyopathy (n=7), adriamycin-induced cardiomyopathy (n=2), and tachycardia-induced cardiomyopathy (n=2). After recovery of LV dysfunction, the patients were followed up for a mean of 41.0±26.3 months. Results：In 9 patients (18%), the LV systolic dysfunction recurred during follow-up (LVEF 32.6±7.3%). There was no significant difference in the baseline clinical and echocardiographic variables between the patients with and without recurrent heart failure. However, cessation of anti-heart failure medication was more frequently observed in the patients with recurrent LV systolic dysfunction (55.6% vs 4.9%, respectively, p<0.05). Conclusion：Recurrent heart failure may ensue in the patients with reversible non-ischemic LV systolic dysfunction. The maintenance of anti-heart failure medication in these patients may be a significant influencing factor for their clinical prognosis. (Korean Circulation J 2006;36:53-59)