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1.
Intern Emerg Med ; 19(2): 577-579, 2024 Mar.
Article in English | MEDLINE | ID: mdl-37751085
4.
Chest ; 145(5): 1064-1070, 2014 May.
Article in English | MEDLINE | ID: mdl-24356904

ABSTRACT

BACKGROUND: Reduced pulmonary arterial compliance (Ca) is a marker of poor prognosis in idiopathic pulmonary arterial hypertension. We tested the hypothesis that pulmonary arterial Ca could be a predictor of outcome in patients with chronic heart failure (CHF). METHODS: We enrolled 306 patients with CHF due to systolic left ventricular dysfunction (sLVD) who underwent a clinically driven right-sided heart catheterization. Pulmonary arterial Ca was measured by the ratio between stroke volume and pulse pressure (SV/PP). The primary end point was cardiovascular death; secondary end point was the composite of cardiovascular death, urgent heart transplantation, and appropriately detected and treated episode of ventricular fibrillation. RESULTS: An inverse relationship was observed between SV/PP and pulmonary vascular resistance, the mean resistance-compliance product (RC-time) being 0.30 ± 0.2 s. In patients with pulmonary capillary wedge pressure (PCWP) < 15 mm Hg, the mean RC-time was 0.34 ± 0.14 s, and in patients with PCWP ≥ 15 mm Hg it was 0.28 ± 0.22 s. Eighty-seven patients died in a follow-up period of 50 ± 32 months. At receiver operating characteristic curve analysis, the optimal prognostic cutoff point of SV/PP was 2.15 mL/mm Hg. An elevated (> 2.15) SV/PP was more strongly associated with survival than any other hemodynamic variable; it was associated with poor prognosis both in patients with high (P = .003) and in patients with normal pulmonary vascular resistance (P = .005). CONCLUSIONS: Pulmonary arterial Ca is a strong prognostic indicator in patients with CHF with sLVD. Most importantly, its prognostic role is retained in patients with normal pulmonary vascular resistance.


Subject(s)
Heart Failure/physiopathology , Pulmonary Wedge Pressure/physiology , Vascular Resistance/physiology , Ventricular Function, Left/physiology , Cardiac Catheterization , Cause of Death/trends , Echocardiography , Female , Follow-Up Studies , Heart Failure/diagnostic imaging , Heart Failure/mortality , Humans , Italy/epidemiology , Male , Middle Aged , Prognosis , Risk Factors , Stroke Volume , Survival Rate/trends
6.
Resuscitation ; 80(4): 493-6, 2009 Apr.
Article in English | MEDLINE | ID: mdl-19231061

ABSTRACT

Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is often challenging due to differing clinical presentations and unpredictable progression of the disease. We report a case of ARVD/C that presented as cardiac arrest in an 18-year-old male while playing soccer. The electrocardiographic features after resuscitation were typical of anterior ST-segment elevation acute myocardial infarction, and the patient was initially managed accordingly. Importantly, an urgent coronary angiogram revealed completely normal coronary arteries. ARVD/C was first suspected following an echocardiogram, and was later confirmed by cardiac magnetic resonance. One month before the event, the patient had been evaluated for ventricular extrasystoles and an abnormal resting electrocardiogram, however ARVD/C was ruled out because of the presence of only two minor diagnostic criteria (T-wave inversion in anterior precordial leads in the absence of right bundle branch block and more than 1000 ventricular extrasystoles during 24-h Holter monitoring). In consequence, physical activity was not forbidden. In conclusion, this case report enforces the need for a strict prohibition of physical activity and serial evaluation of individuals with only minor diagnostic criteria for ARVD/C, for lacking sensibility of Task Force diagnostic criteria.


Subject(s)
Arrhythmogenic Right Ventricular Dysplasia/complications , Arrhythmogenic Right Ventricular Dysplasia/diagnosis , Myocardial Infarction/etiology , Adolescent , Arrhythmogenic Right Ventricular Dysplasia/physiopathology , Electrocardiography , Humans , Male , Myocardial Infarction/diagnosis , Myocardial Infarction/physiopathology
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