Lung Ultrasound-Implemented Diagnosis of Acute Decompensated Heart Failure in the ED: A SIMEU Multicenter Study.

BACKGROUND: Lung ultrasonography (LUS) has emerged as a noninvasive tool for the differential diagnosis of pulmonary diseases. However, its use for the diagnosis of acute decompensated heart failure (ADHF) still raises some concerns. We tested the hypothesis that an integrated approach implementing LUS with clinical assessment would have higher diagnostic accuracy than a standard workup in differentiating ADHF from noncardiogenic dyspnea in the ED. METHODS: We conducted a multicenter, prospective cohort study in seven Italian EDs. For patients presenting with acute dyspnea, the emergency physician was asked to categorize the diagnosis as ADHF or noncardiogenic dyspnea after (1) the initial clinical assessment and (2) after performing LUS ("LUS-implemented" diagnosis). All patients also underwent chest radiography. After discharge, the cause of each patient's dyspnea was determined by independent review of the entire medical record. The diagnostic accuracy of the different approaches was then compared. RESULTS: The study enrolled 1,005 patients. The LUS-implemented approach had a significantly higher accuracy (sensitivity, 97% [95% CI, 95%-98.3%]; specificity, 97.4% [95% CI, 95.7%-98.6%]) in differentiating ADHF from noncardiac causes of acute dyspnea than the initial clinical workup (sensitivity, 85.3% [95% CI, 81.8%-88.4%]; specificity, 90% [95% CI, 87.2%-92.4%]), chest radiography alone (sensitivity, 69.5% [95% CI, 65.1%-73.7%]; specificity, 82.1% [95% CI, 78.6%-85.2%]), and natriuretic peptides (sensitivity, 85% [95% CI, 80.3%-89%]; specificity, 61.7% [95% CI, 54.6%-68.3%]; n = 486). Net reclassification index of the LUS-implemented approach compared with standard workup was 19.1%. CONCLUSIONS: The implementation of LUS with the clinical evaluation may improve accuracy of ADHF diagnosis in patients presenting to the ED. TRIAL REGISTRY: Clinicaltrials.gov; No.: NCT01287429; URL: www.clinicaltrials.gov.

Anti-hypertensive drugs and left ventricular hypertrophy: a clinical update.

Structural remodelling of the heart, known as left ventricular hypertrophy (LVH), is a consequence of systemic hypertension, and is associated with an increased risk of cardiovascular morbidity and mortality. Therefore, particular attention should be paid to the identification, prevention and treatment of this condition in hypertensive patients. LVH seems to benefit from all classes of anti-hypertensive drugs; however, antagonists of the renin-angiotensin-aldosterone system (RAAS) have demonstrated an additional benefit in the inhibition and reversal of myocardial interstitial fibrosis. Nevertheless, in evaluating the degree of arterial hypertension and organ damage, many neuro-hormonal systems are involved, primarily the sympathetic nervous system, thereby explaining the use of different classes of anti-hypertensive drugs to prevent or reduce LVH. The RAAS antagonists are actually the recommended anti-hypertensive agents to prevent organ damage in hypertensive subjects or in hypertensives with evidence of LVH to reduce cardiovascular mortality and morbidity.

Baroreflex sensitivity correlates with left ventricular morphology and diastolic function in essential hypertension.

OBJECTIVES: Arterial hypertension is a common cause of cardiac organ damage, inducing morphological and functional modifications. Spontaneous baroreflex sensitivity (BRS) control of the heart rate is a key mechanism of blood pressure homeostasis, and is impaired in patients with hypertension. This study sought to assess the association between BRS and left ventricular morphology and function. METHODS: We studied 224 hypertensive patients (125 men; aged 47.8 +/- 10.8 years, mean +/- SD) compared with 51 normotensive control subjects (25 men, aged 45.7 +/- 12.5 years). Left ventricular morphology, systolic and diastolic function were evaluated by echocardiography. Spontaneous BRS was measured using the sequence method. RESULTS: BRS was inversely associated with relative wall thickness (R = 0.17; P < 0.0001) and left ventricular mass index (R = 0.03; P = 0.01); in particular, BRS was significantly impaired in patients with concentric left ventricular remodelling (median [interquartile difference] 9.4 [4.1]) and hypertrophy (9.05 [3.9]) compared with the normal left ventricle (12.3 [5]; P < 0.001). BRS showed a significant association with systolic function evaluated by midwall fractional shortening (r = 0.28; P < 0.001), stroke volume (r = 0.27; P < 0.001), stroke work (r = 0.17; P < 0.05), and fractional shortening (r = 0.17; P < 0.05). BRS was significantly decreased in patients with diastolic dysfunction; it was lower in patients with diastolic dysfunction compared with both the control group and hypertensive patients with normal diastolic function. CONCLUSION: BRS is associated with left ventricular morphology, systolic and diastolic function in hypertensive patients. In particular BRS is impaired in patients with diastolic dysfunction. These findings suggest a role for BRS as a target in arterial hypertension.