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Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay.

BACKGROUND: One third of patients with chronic heart failure have electrocardiographic evidence of a major intraventricular conduction delay, which may worsen left ventricular systolic dysfunction through asynchronous ventricular contraction. Uncontrolled studies suggest that multisite biventricular pacing improves hemodynamics and well-being by reducing ventricular asynchrony. We assessed the clinical efficacy and safety of this new therapy. METHODS: Sixty-seven patients with severe heart failure (New York Heart Association class III) due to chronic left ventricular systolic dysfunction, with normal sinus rhythm and a duration of the QRS interval of more than 150 msec, received transvenous atriobiventricular pacemakers (with leads in one atrium and each ventricle). This single-blind, randomized, controlled crossover study compared the responses of the patients during two periods: a three-month period of inactive pacing (ventricular inhibited pacing at a basic rate of 40 bpm) and a three-month period of active (atriobiventricular) pacing. The primary end point was the distance walked in six minutes; the secondary end points were the quality of life as measured by questionnaire, peak oxygen consumption, hospitalizations related to heart failure, the patients' treatment preference (active vs. inactive pacing), and the mortality rate. RESULTS: Nine patients were withdrawn from the study before randomization, and 10 failed to complete both study periods. Thus, 48 patients completed both phases of the study. The mean distance walked in six minutes was 22 percent greater with active pacing (399+/-100 m vs. 326+/-134 m, P<0.001), the quality-of-life score improved by 32 percent (P<0.001), peak oxygen uptake increased by 8 percent (P<0.03), hospitalizations were decreased by two thirds (P<0.05), and active pacing was preferred by 85 percent of the patients (P<0.001). CONCLUSIONS: Although it is technically complex, atriobiventricular pacing significantly improves exercise tolerance and quality of life in patients with chronic heart failure and intraventricular conduction delay.

Angiotensin-Converting Enzyme Inhibitors↗

Influence of beta-blockers on mortality in chronic heart failure.

OBJECTIVE: To briefly discuss the pathophysiology of heart failure and the rationale for the use of beta-blockers in the treatment of chronic heart failure. Key morbidity reduction trials are briefly mentioned, and recent mortality reduction trials are reviewed. General recommendations regarding the use of beta-blockers in heart failure are also included to guide clinical practice. STUDY SELECTION/DATA EXTRACTION: Randomized, placebo-controlled clinical trials and meta-analyses evaluating mortality reduction with beta-blockers in the treatment of heart failure were identified using a MEDLINE search from January 1993 to March 2000. Abstracts and presented results from recent scientific meetings were also considered. DATA SYNTHESIS: Beta-blockers have been shown to decrease hospitalization for worsening heart failure, decrease the need for heart transplant, improve New York Heart Association (NYHA) functional class, and increase left-ventricular ejection fraction. A mortality benefit has recently been demonstrated for patients with chronic heart failure. Carvedilol, bisoprolol, and controlled-release/extended-release metoprolol decreased the risk of dying by 65%, 34%, and 34%, respectively, in patients with primarily NYHA functional class II or III and systolic dysfunction. The benefit of these agents in patients with class IV heart failure or determining whether one agent has an advantage over another is being investigated in ongoing clinical trials. CONCLUSIONS: Several beta-blockers have demonstrated mortality reduction in the treatment of patients with NYHA functional class II or III heart failure and systolic dysfunction. Beta-blockers should be considered in these patients when they are clinically stable and taking the current standard therapy of a diuretic plus an angiotensin-converting enzyme inhibitor or other vasodilator agent.

Adrenergic beta-Antagonists↗

Echocardiographic predictors of stroke in patients with atrial fibrillation: a prospective study of 1066 patients from 3 clinical trials.

BACKGROUND: Clinical features that consistently predict ischemic stroke in patients with nonvalvular atrial fibrillation have been identified, while echocardiographic risk factors are less well defined. OBJECTIVE: To determine whether the results of transthoracic echocardiography add independent information to the clinical risk factors for stroke in patients with atrial fibrillation. METHODS: Transthoracic echocardiographic findings and clinical features from 1066 patients with atrial fibrillation assigned to placebo or control in 3 randomized trials (Boston Area Anticoagulation Trial for Atrial Fibrillation, Stroke Prevention in Atrial Fibrillation I Study, and Veterans Affairs Prevention in Atrial Fibrillation Study) were correlated with subsequent ischemic stroke by multivariate analysis. RESULTS: The mean + SD age of patients was 67 +/- 10 years, 78% were men, 55% had a history of hypertension, 19% had a history of diabetes, 7% had a previous transient ischemic attack or stroke, and 27% had a history of heart failure. During a mean follow-up of 1.6 years, 78 ischemic strokes occurred (annual rate, 4.7%). Moderate to severe left ventricular systolic dysfunction shown via 2-dimensional echocardiography was a strong independent predictor of stroke (relative risk, 2.5; P<.001) in the 1010 patients in whom echocardiographic values for left ventricular function were available. Left atrial diameter by M-mode echocardiography did not predict stroke (relative risk, 1.02/mm; P = .10). Of 163 patients categorized as low risk based on clinical features (annual stroke rate, 0.8%; 95% confidence interval, 0.2%-3.0%), 10 had moderate to severe left ventricular dysfunction shown via 2-dimensional echocardiography and a 9.3% per year risk of stroke (95% confidence interval, 1.3%-66%). Conversely, 728 of the 847 patients at high risk for stroke based on clinical criteria had normal or mildly abnormal left ventricular function; their stroke rate was 4.4% (95% confidence interval, 3.4%-5.8%). CONCLUSIONS: Left ventricular systolic dysfunction shown via 2-dimensional transthoracic echocardiography independently predicts risk of stroke in patients with atrial fibrillation. Echocardiography may prove most useful in a small group of patients who have a low risk of stroke according to clinical factors.

Aged↗

Fetal cardiomyopathies: pathogenic mechanisms, hemodynamic findings, and clinical outcome.

BACKGROUND: Although the prenatal diagnosis of most fetal structural heart defects and dysrhythmias has been described, there is a paucity of information about cardiomyopathies (CMs) in prenatal life. METHODS AND RESULTS: To determine the pathogenic mechanisms, hemodynamic findings, and outcome of fetal CM, we reviewed the fetal echocardiograms and perinatal histories of 55 affected fetuses. Dilated CM was diagnosed in 22 cases, including 2 with congenital infections, 5 familial cases, 6 with endocardial fibroelastosis related to maternal anti-Ro/La antibodies, and 9 idiopathic cases. Thirty-three had hypertrophic CM, 7 associated with maternal diabetes, 2 with Noonan's syndrome, 2 with alpha-thalassemia, 18 with twin-twin transfusion syndrome, 1 with familial hypertrophy, and 3 with idiopathic hypertrophy. Systolic dysfunction was present in all cases of dilated CM and 15 cases of hypertrophic CM. Diastolic dysfunction was present in 19 of 30 fetuses with assessment of diastolic function parameters. Significant mitral or tricuspid valve regurgitation was seen in 32 cases. Eight fetuses were hydropic and 23 had signs of early hydrops. Seven pregnancies were terminated. Of 46 continued pregnancies with follow-up, 29 (63%) died perinatally. The presence of systolic dysfunction, diastolic dysfunction, and significant atrioventricular valve regurgitation were identified as risk factors for mortality. By multiple logistic regression, diastolic dysfunction was associated with an 8-fold increased risk relative to the other parameters. CONCLUSIONS: Fetal CM has a broad spectrum of intrinsic and extrinsic causes. A poor outcome is observed in many affected fetuses. Diastolic dysfunction in fetal CM is associated with the highest risk of mortality.

Cardiomyopathies↗

Left ventricular function in acute hypothyroidism: a Doppler echocardiography study.

BACKGROUND: Acute changes in cardiac parameters may occur after L-thyroxine withdrawal in patients totally thyroidectomized for thyroid cancer. The literature data regarding cardiac function in acute hypothyroidism are limited and discordant. METHODS: In order to evaluate the effects of acute hypothyroidism on cardiac function, 20 athyreotic patients (3 males, 17 females, mean age 46.4 +/- 8.6 years, range 18-58 years) underwent Doppler echocardiography during L-thyroxine therapy (euthyroid phase) and 5 weeks after hormone therapy withdrawal (hypothyroid phase). RESULTS: Significant changes in the left ventricular mass (83 +/- 12 vs 93 +/- 17 g/m2, p = 0.004) and end-diastolic volume (56 +/- 9 vs 50 +/- 9 ml/m2, p = 0.01) were found. Among systolic function parameters, the pre-ejection period/left ventricular ejection time (PEP/LVET) ratio (0.33 +/- 0.07 vs 0.40 +/- 0.08, p = 0.0002), aortic peak flow velocity corrected for heart rate (3.9 +/- 0.7 vs 3.5 +/- 0.5 cm/s, p = 0.02) and mean aortic acceleration corrected for heart rate (45 +/- 15 vs 38 +/- 9 cm/s2, p = 0.007) showed significant variations, whereas the left ventricular fractional shortening (39 +/- 5 vs 40 +/- 6%, p = NS) and ejection fraction (69 +/- 6 vs 68 +/- 7%, p = NS) did not change. Among diastolic function parameters, only the E-wave velocity decreased (73 +/- 17 vs 65 +/- 12 cm/s, p = 0.01); no significant modification was found in the A-wave velocity (62 +/- 19 vs 58 +/- 14 cm/s, p = NS), E/A ratio (1.2 +/- 0.5 vs 1.1 +/- 0.3, p = NS), isovolumic relaxation time (93 +/- 16 vs 95 +/- 37 ms, p = NS) and E-wave deceleration time (233 +/- 48 vs 235 +/- 45 ms, p = NS). The pattern of left ventricular filling remained unchanged, except in 2 patients. The Suga-Sagawa's index, a known parameter of myocardial contractility, was unchanged (5.6 +/- 2 vs 6.1 +/- 2 mmHg/ml, p = NS). The systemic vascular resistance increased (1511 +/- 599 vs 2216 +/- 408 dynes-s-cm(-5), p = 0.002), while the stroke index (39 +/- 8 vs 33 +/- 7 ml/m2, p = 0.001) and cardiac index (2.74 +/- 0.6 vs 2.07 +/- 0.5 l/min/m2, p = 0.0001) significantly decreased. CONCLUSIONS: Acute hypothyroidism was associated with left ventricular systolic dysfunction, probably due to pre- and afterload alterations rather than to an impaired myocardial contractility. The diastolic function was not significantly modified. An increase in cardiac mass was also found, possibly a consequence of early interstitial myxedema. Unlike the PEP/LVET ratio, both the fractional shortening and ejection fraction may be unreliable indicators of left ventricular systolic dysfunction in patients with acute hypothyroidism.

Acute Disease↗

[ACE inhibitors and/or sartans in heart failure: is there a difference?].

The recent years have witnessed tremendous advances in the understanding of the pathophysiology of chronic heart failure (CHF), leading to significant improvement in therapy. Recognition of the deleterious effects of angiotensin II is an major therapeutic target. By blocking the transformation of angiotensin I to angiotensin II, angiotensin-converting enzyme inhibitors (ACEI) improve symptoms, exercise tolerance and survival at all stages of CHF. Angiotensin II-receptors blockers (ARB) have several theoretical advantages over ACEI, including a better tolerance profile, that may lead to a more favourable effect. In CHF with systolic dysfunction, randomised-controlled trials comparing losartan to captopril (ELITE 1 and ELITE 2) or valsartan versus placebo on top of conventional therapy (Val-HeFT) failed to demonstrate a superiority of ARB's compared to ACEI in terms of mortality. However, ARB's appeared better tolerated in this indication. The treatment of CHF with preserved systolic function remains unclear and may be defined in a near future by two studies addressing the role of on candesartan (CHARM study) or irbesartan (I-Preserve study) in this form of CHF. ACEI and beta-blockers remain on first line for treating CHF due to systolic dysfunction. Losartan or valsartan can be considered as an alternative if ACEI are not tolerated or contraindicated.

Angiotensin Receptor Antagonists↗

Utility of various radionuclide techniques for distinguishing ischemic from nonischemic dilated cardiomyopathy.

BACKGROUND: Clinically, ischemic and nonischemic (idiopathic) dilated cardiomyopathy may be difficult to distinguish. Radionuclide ventriculography and exercise testing with thallium-201 scintigraphy are often used in an attempt to differentiate them noninvasively. With these techniques, the presence of (1) left ventricular (LV) regional asynergy, (2) depressed LV systolic function with normal right ventricular function, and/or (3) thallium-201 perfusion abnormalities traditionally has been regarded as evidence of ischemic heart disease. We assessed the incidence with which these abnormalities occur in patients with nonischemic-dilated cardiomyopathy. METHODS: Seventy-six patients (45 men, 31 women, aged 18 to 75 years) with invasively proven nonischemic-dilated cardiomyopathy underwent radionuclide ventriculography (n = 75) and provocative thallium-201 perfusion imaging (n = 17). RESULTS: Regional LV wall motion abnormalities were noted in 48% of patients, and 54% had LV systolic dysfunction without concomitant right ventricular dysfunction. Reversible and/or fixed exercise-induced thallium-201 perfusion abnormalities occurred in 94% of the patients studied. CONCLUSIONS: Radionuclide ventriculography and exercise testing with thallium perfusion imaging cannot be used reliably to differentiate ischemic from nonischemic dilated cardiomyopathy, since many patients with the latter have radionuclide evidence of LV segmental wall motion abnormalities, selective LV systolic dysfunction, and segmental perfusion abnormalities.

Adolescent↗

Thromboembolism in heart failure: who should be treated?

The risk of thromboembolic complications in patients with heart failure and/or chronic left-ventricular systolic dysfunction is increased. Nevertheless, anticoagulant therapy in these patients is still a subject of debate. Atrial fibrillation is the only prospectively evaluated, proven thromboembolic risk factor and patients with atrial fibrillation benefit from long term anticoagulant therapy. The significance of other proposed thromboembolic risk factors in heart failure and/or chronic left-ventricular dysfunction such as gender, cause of myocardial disease, severity of heart failure, left-ventricular ejection fraction, left-ventricular thrombus, left ventricular aneurysm and history of previous thromboembolic event is less clear. This article summarizes key studies, assesses the incidence of thromboembolism, evaluates risk factors and proposes guidelines for anticoagulation of patients with heart failure and/or left ventricular systolic dysfunction.

Adult↗

The carvedilol hibernation reversible ischaemia trial; marker of success (CHRISTMAS). The CHRISTMAS Study Steering Committee and Investigators.

BACKGROUND: Carvedilol improves left ventricular (LV) function when heart failure is due to LV systolic dysfunction, but the magnitude of the response is heterogeneous among patients with coronary disease, possibly reflecting the presence or volume of hibernating myocardium. AIMS: The primary objective of the study is to determine whether the presence of hibernating myocardium predicts the magnitude of improvement in LV ejection fraction in response to carvedilol among patients with heart failure and LV systolic dysfunction due to coronary disease. METHODS: The study is a prospective, randomised, parallel-group, double-blind, multi-centre study comparing carvedilol and placebo over a period of approximately 6 months in the above patient population. The primary end-point is the comparison of the mean change, from baseline to the final visit, in radionuclide-determined LV ejection fraction among patients on placebo with those on carvedilol stratified according to the presence of hibernating myocardium. Hibernating status will be determined by a combination of echocardiographic and myocardial perfusion (technetium-99m sestamibi) imaging. RESULTS: 255 patients have undergone screening tests of which 207 have been randomised so far. The study intends to randomise 400 patients and the first report of results is expected in 2000. CONCLUSIONS: As far as we are aware this is the first randomised controlled trial to investigate the effects of treatment in patients stratified according to the presence of hibernating myocardium. The study will provide insights into the prevalence of myocardial hibernation, its natural history, and its influence on prognosis as well as the interaction between the presence of hibernating myocardium and the effects of treatment with carvedilol.

Adrenergic beta-Antagonists↗

beta-blockers in heart failure: recently completed and ongoing clinical trials.

beta-Blockers have emerged as an important therapy in patients with symptomatic left ventricular systolic dysfunction. Early studies demonstrated that beta-blocker therapy improved left ventricular function, reduced neurohumoral activity and reduced heart failure symptoms in these patients. While none of these small studies demonstrated a significant benefit in terms of overall survival, several meta-analyses suggested that beta-blocker therapy could, in fact, reduce mortality in patients with left ventricular systolic dysfunction and mild to moderate heart failure symptoms (New York Heart Association class II or III). Three large, recently completed, trials have confirmed the benefit of beta-blockade in these patients. This report reviews some of the initial clinical studies of beta-blockade in heart failure, examines the findings of the three large multicentre trials and other relevant research. Finally, ongoing trials designed to assess the relative efficacy of different beta-blockers and evaluate the utility of beta-blockade in specific subsets of patients with heart failure are discussed.

Adrenergic beta-Antagonists↗

Superoxide dismutase activity in adriamycin-induced cardiotoxicity in humans: a potential novel tool for risk stratification.

BACKGROUND: Oxidative stress has been implicated in Adriamycin cardiotoxicity experimentally. We evaluated whether changes in systemic markers of antioxidant reserve occur and are associated with left ventricular (LV) dysfunction during Adriamycin use in humans. METHODS AND RESULTS: We prospectively evaluated oncology patients eligible for Adriamycin chemotherapy. Blood samples for enzymatic (erythrocyte superoxide dismutase activity [SOD-U SOD/mg protein]) and nonenzymatic antioxidants (total radical trapping antioxidant potential [TRAP-U of Trolox/microL plasma]) were collected at baseline (B), intermediate (I), and final (F) cycles. LV ejection fraction (LVEF) was assessed by radionuclide ventriculography. Fifty-one patients (49 +/- 12 years, 90% female) underwent 5.9 +/- 0.9 chemotherapy cycles and received 301 +/- 52 mg/m 2 of Adriamycin. LVEF decreased from 61 +/- 6% (B) to 56 +/- 7% (F) ( P < .001), but only 6 (12%) patients developed significant LV systolic dysfunction (LVEF < 50%). SOD activity increased significantly during treatment (4.5 +/- 1.8 [B], 6.0 +/- 2.1 [I], 5.6 +/- 2.2 [F]; P < .01), whereas TRAP values were unchanged. Baseline SOD activity from patients who developed LV systolic dysfunction was significantly higher than from those who maintained normal LVEF (5.9 +/- 1.8 versus 4.3 +/- 1.7; P < .05). In multivariate analysis, baseline SOD levels remained independently associated with LV dysfunction ( P = .05). CONCLUSION: Erythrocyte SOD activity increases after Adriamycin treatment and high baseline levels predicts Adriamycin-induced cardiotoxicity in humans.

Antibiotics, Antineoplastic↗

Hemodynamic and volume correlates of left ventricular diastolic relaxation and filling in patients with aortic stenosis.

OBJECTIVE: The aim of the present study was to evaluate the hemodynamic and volume correlates of early diastolic filling and isovolumetric relaxation in patients with aortic stenosis. BACKGROUND: Left ventricular diastolic relaxation and filling have been found to be heterogeneous in patients with aortic stenosis. Potential mechanisms underlying this heterogeneity include individual differences in the severity of muscle hypertrophy or systolic dysfunction, or both, in the presence and severity of mitral regurgitation and in the level of left atrial pressure. METHODS: Right (fluid-filled) and left (high fidelity micromanometer) ventricular pressures, left ventricular volumes (contrast angiography) and transmitral inflow dynamics (Doppler echocardiography) were measured in 17 patients with isolated severe aortic stenosis (valve area less than 0.75 cm2). Measurements included left ventricular end-diastolic and end-systolic volumes, left ventricular ejection fraction, peak positive and negative first derivative of left ventricular pressure (dP/dt), the time constant of isovolumetric relaxation (tau), left ventricular end-diastolic pressure, left ventricular mass, left ventricular end-systolic stress, mean capillary wedge pressure and peak early (E) and late (A) transmitral filling velocities. Patients were subclassified according to left ventricular ejection performance at rest and mean capillary wedge pressure. RESULTS: Patients with normal ejection performance and normal mean capillary wedge pressure had a normal rate of isovolumetric left ventricular pressure decay and an abnormal diastolic filling pattern, with diastolic filling occurring primarily during atrial systole. In contrast, in patients with systolic dysfunction and elevated mean capillary wedge pressure, isovolumetric pressure decay was prolonged and diastolic filling occurred essentially during the rapid filling period, with reduced atrial contribution to left ventricular filling and a short isovolumetric relaxation period. Stepwise multiple linear regression analysis identified two variables as independent predictors of transmitral velocity profile and three variables independently predictive of the rate of left ventricular pressure decay. The single most important predictor of transmitral filling pattern was the pulmonary capillary wedge pressure (p less than 0.0001), followed by the left ventricular peak negative dP/dt (p = 0.002). The single most powerful predictor of the rate of reduction in left ventricular pressure was left ventricular mass index (p less than 0.0001), followed by end-systolic volume index (p = 0.0002) and left ventricular peak negative dP/dt (p = 0.0029). CONCLUSIONS: In patients with aortic stenosis, left ventricular filling is essentially determined by left atrial pressure, whereas isovolumetric relaxation more closely depends on the severity of muscle hypertrophy and chamber dilation.

Aged↗

Angiotensin-converting enzyme inhibitors in left ventricular dysfunction.

Angiotensin-converting enzyme (ACE) inhibitors have been used for more than a decade in the treatment of chronic congestive heart failure. In recent years these agents have been used in patients who survived a myocardial infarction. However, primary care providers are often confused as to which patients would benefit the most, and as a result, these life-prolonging drugs are underutilized. The results of randomized controlled trials evaluating ACE inhibitors' effect on morbidity and mortality in patients with chronic congestive heart failure or acute myocardial infarction were evaluated. Angiotensin-converting enzyme inhibitors clearly improve survival in patients with symptomatic congestive heart failure. This survival benefit is approximately 6 months. In patients with asymptomatic systolic dysfunction, these agents also decrease the number of hospital admissions due to heart failure. Angiotensin-converting enzyme inhibitors also improve survival in all patients who experienced an acute myocardial infarction. With the plethora of evidence regarding the positive effects that this class of drugs has on the quality of life and survival of patients with systolic dysfunction, it is still unclear why clinicians are reluctant to use them more often. Primary care providers need to be educated on how to risk stratify patients to make this therapy more cost effective, and when these agents should be started.

Angiotensin-Converting Enzyme Inhibitors↗

Idiopathic enlargement of the right atrium: 23 year follow up of a familial cluster and their unaffected relatives.

OBJECTIVE: To evaluate the long term outcome of familial idiopathic enlargement of the right atrium (IERA) and the risk of developing this disorder among unaffected offspring. DESIGN: 23 year follow up study. PATIENTS: 14 members (eight men, mean age 54 years, range 40-78) of a pedigree with familial IERA. METHODS: All patients were examined clinically and echocardiographically in 1979 and 2002. Normal cross sectional dimensions of the right atrium were derived from echocardiographic evaluation of 100 people (47% men) with no structural or haemodynamic signs of heart disease. The 90th centile was chosen as the upper normal limit. IERA was defined as an increased right atrial long axis indexed to body surface area (RALAX(i), men > 2.6 cm/m2, women > 2.8 cm/m2) in the absence of other cardiac abnormalities. Severe IERA was defined arbitrarily as RALAX(i) > or = 4 cm/m2. RESULTS: The course of the two index patients with severe IERA diagnosed in 1979 was complicated by atrial fibrillation, systemic embolism, and symptoms of heart failure without systolic dysfunction, resulting in the death of one man (77 years old). One of two patients with initially mild forms progressed to severe IERA. All of the initially unaffected offspring (n = 9) remained asymptomatic, although four of them had developed mild IERA. CONCLUSIONS: During 23 years' follow up, severe IERA induced atrial fibrillation, systemic embolism, and symptoms of heart failure without systolic dysfunction in all cases in this family. Mild IERA seems to become manifest during middle age and may be followed by gradual progression to clinically relevant disease.

Adult↗

Age and gender differences in left ventricular function among patients with stable angina and a matched control group. A report from the Angina Prognosis Study in Stockholm.

To assess left ventricular systolic and diastolic function, M-mode (n = 675) and transmitral Doppler echocardiography (n = 358) were performed in patients with stable angina pectoris and compared with 50 matched healthy controls. Left ventricular fractional shortening (FS) was significantly lower in male than in female patients (32 +/- 7 vs. 35 +/- 7%, p < 0.001). A history of heart failure was as frequent in men (6%) as in women (6%), but left ventricular systolic dysfunction was more frequent in men than in women (25 vs. 12%, p < 0.005). The ratio of early/late diastolic peak flow velocity (E/A ratio) was significantly lower, indicating diastolic dysfunction, in female patients with clinical heart failure than in those without (0.79 +/- 0.25 vs. 1.02 +/- 0.3, p < 0.05). No such difference was found in male patients. Inverse relationships were found between age and E/A ratio in both controls (r = -0.45, p < 0.001) and angina patients (r = -0.44, p < 0.001). Thus, despite similar frequency of clinical heart failure, left ventricular systolic dysfunction was more common in men than in women with stable angina.

Adrenergic beta-Antagonists↗

Echocardiographic findings in a contemporary Afro-Caribbean population referred for evaluation of atrial fibrillation or flutter.

Atrial fibrillation and/or flutter is the most common and the most significant cardiac arrhythmia in the Caribbean. This study is an attempt to determine the echocardiographic findings in a current, consecutive series of Afro-Caribbean patients referred for evaluation of atrial fibrillation and flutter. Between May 1998 and June 2000, 50 patients (mean age 67 years, 58% male) had echocardiograms done. Measurements included left atrial dimension (LA), left ventricular end-systolic dimension (LVESD), LV end-diastolic dimension (LVEDD), LV posterior wall thickness (LVPWT) and ventricular septal thickness (VST). Left ventricular ejection fraction (EF) was calculated. LA > 4 cm, LVPWT or VST > 13 mm, and LVEF < 50% were considered abnormal. Atrial fibrillation was seen in 92%, atrial flutter in 8%; 60% were chronic, 40% paroxysmal; 56% had congestive heart failure. The most frequent echocardiographic finding was LV hypertrophy (19/50, 38%). Left ventricular systolic dysfunction was present in 12/50, 24% (25% with LV hypertrophy also). Valvular disease (abnormal appearing valve, no Doppler study), was seen in 9/50, 18%. Normal findings ("lone atrial fibrillation") were seen in 10/50, 20%. Increased LA dimension was seen in 39/50, 78%. Patients with lone atrial fibrillation were younger (mean 56 years) than those with valvular disease (mean 64 years), LV systolic dysfunction (mean 69 years) and those with LV hypertrophy (mean 72 years). Thus, LV hypertrophy, probably secondary to hypertension, is the most frequent echocardiographic finding, with LV dysfunction (such as seen in coronary artery disease) seen less often. Valvular disease and lone atrial fibrillation rates are similar to rates in developed countries.

Adolescent↗

Diastolic heart failure: neglected or misdiagnosed?

Recent epidemiological studies suggest that 30% to 50% of patients with heart failure (HF) have preserved left ventricular (LV) systolic function. These patients, often presumed to have diastolic heart failure (DHF), appear to have lower short-term but similar long-term mortality when compared to patients with HF and LV systolic dysfunction. Rates of recurrent hospitalization and costs of care appear similar in the two groups of patients. Therefore, DHF may contribute significantly to the burden of disease caused by HF. Exertional breathlessness, the principal symptom of HF, has many causes, including obesity, pulmonary disease and myocardial ischemia. A diagnosis of DHF by exclusion, based on symptoms in the absence of important LV systolic dysfunction or major valve disease, is unsatisfactory. Unfortunately, as yet, no reliable definition with which to make a positive diagnosis of DHF has been agreed on, frequently rendering this diagnosis uncertain. Echocardiography has several limitations, whereas hemodynamic confirmation of DHF by cardiac catheterization is potentially complex and not practically feasible for many patients. Treatment of DHF remains empirical and unsatisfactory because of the lack of large-scale randomized controlled trials in this area. Currently, three large outcome studies on DHF are in progress along with other smaller trials. These should start to provide some of the answers we need to diagnose and effectively treat DHF.

Diastole↗

Reduced forward output states affect the left ventricular opacification of intravenously administered Albunex.

Albunex is an Food and Drug Administration-approved ultrasound contrast agent used for the enhancement of left ventricular endocardial borders. To determine the efficacy of intravenously administered Albunex with regard to left ventricular opacification (LVO), a retrospective analysis of 117 patients who received 202 injections of Albunex for enhancement of endocardial borders was done (dose 0.08 to 0.22 ml /kg). Patients were routinely referred to our echocardiography laboratory for stress echocardiography for standard indications. Optimized settings for contrast enhancement (3.5 MHz transducer frequency and maximum dynamic range) were used. Four observers graded LVO on a scale from 0 to 3 (0 = no Albunex seen in the ventricular cavity; 3 = Albunex densely seen in the ventricular cavity). Overall, LVO was reported in 166 (82%) of 202 injections or in 91 (78%) of 117 patients. A significant reduction in LVO was noted in patients with mitral regurgitation, tricuspid regurgitation, atrial fibrillation, systolic dysfunction, or pulmonary hypertension (increased pulmonary artery systemic pressure). LVO was seen in 88% of the patients without these conditions. However, only 12 (44%) of 27 patients with one or more of the above conditions had LVO (p < 0.05). LVO can be achieved in the majority of patients after intravenously administered Albunex when imaged with optimal transducer settings. A subset of patients with systolic dysfunction, mitral regurgitation, tricuspid regurgitation, atrial fibrillation, or increased pulmonary artery systemic pressure has less effective LVO with Albunex. Heart disease associated with decreased forward flow appears to be associated with diminished LVO.

Adult↗