Clinical, historical and diagnostic findings associated with right ventricular dysfunction in patients with central and non-massive pulmonary embolism.

Right ventricular dysfunction during acute pulmonary embolism (PE) predisposes to hemodynamic instability and cardiogenic shock. Aim of this case-control study was to determine the clinical, historical and diagnostic findings associated with right ventricular dysfunction in patients with acute PE involving the main or segmental pulmonary arteries (central PE) and without hemodynamic instability on admission to the Emergency Department (ED) (non-massive PE). From January 1, 2002 to December 31, 2005, 211 patients with central PE were admitted to the Department of Emergency Medicine of the "Antonio Cardarelli" Hospital (Naples, Italy). One hundred eighteen of them had echocardiographic evidence of right ventricular dysfunction on admission to the ED. A history of type 2 diabetes mellitus and chronic obstructive pulmonary disease were significantly associated with an increased risk of this PE-related complication. Compared to patients without right ventricular dysfunction, those with right ventricular dysfunction showed higher levels of markers of cardiac damage, and a significant impairment of respiratory function. Echocardiographic evidence of right ventricular dysfunction on admission to the ED was significantly associated with the occurrence of hemodynamic instability and cardiogenic shock during the PE clinical course. The study results indicate that a history of type 2 diabetes mellitus and chronic obstructive pulmonary disease are significantly associated with the occurrence of right ventricular dysfunction in patients with non-massive and central PE independent of age, gender and other historical and clinical variables detectable on admission to the ED.

Predictors of in-hospital and long-term clinical outcome in elderly patients with massive pulmonary embolism receiving thrombolytic therapy.

OBJECTIVES: To determine the clinical, historical, and instrumental findings associated with unfavorable short-term and long-term prognosis in elderly patients (>or=65) receiving thrombolytic therapy for pulmonary embolism (PE). DESIGN: Case-control retrospective study. SETTING: General medicine acute care ward. PARTICIPANTS: Sixty-seven elderly patients with PE complicated by hemodynamic instability (massive PE) admitted to the "Antonio Cardarelli" Hospital from January 1, 2002, to December 31, 2004, and evaluated during their hospital stay and 174.4+/-4.6 days after discharge. MEASUREMENTS: PE diagnosis was confirmed using spiral computed tomography angiography. Hemodynamic instability was defined as cardiogenic shock and systolic blood pressure less than 90 mmHg or a pressure drop of 40 mmHg or more for longer than 15 minutes not due to new-onset arrhythmia, hypovolemia, or sepsis. INTERVENTION: Weight-adapted unfractionated heparin and recombinant tissue plasminogen activator. RESULTS: Nine patients (13.4%) died during hospitalization. Higher troponin-I (cTn-I) serum levels at admission to the emergency department and the occurrence of thrombocytopenia after thrombolysis were significantly associated with in-hospital death. Nineteen of the 58 survivors (32.7%) died during follow-up. The risk factors for long-term death were historical findings of cancer and cardiovascular disease at hospital admission. CONCLUSION: Higher cTn-I serum levels in the acute phase and the occurrence of thrombocytopenia after thrombolysis were significantly associated with in-hospital mortality in elderly patients with massive PE. In the same setting, historical findings of cancer and cardiovascular disease are strong predictors of death in the long term.

Increased troponin I predicts in-hospital occurrence of hemodynamic instability in patients with sub-massive or non-massive pulmonary embolism independent to clinical, echocardiographic and laboratory information.

INTRODUCTION: Whether in patients with acute central sub-massive or non-massive pulmonary embolism, mild troponin I increase (>0.03 mug/L) predicts in-hospital occurrence of hemodynamic instability and death independent to prognostically relevant clinical, laboratory and echocardiographic information is not fully established. METHODS AND RESULTS: We evaluated consecutively patients admitted to the Emergency Room for pulmonary embolism; those in stable hemodynamics in whom central pulmonary embolism was confirmed by spiral-computed tomography were recruited. All participants underwent standardized study protocol, including clinical and diagnostic evaluation for assessment of severity of pulmonary embolism; therapy was established accordingly; troponin I was measured, but treatment protocol was not affected by knowledge of troponin I levels. Of 90 patients enrolled in the study, 33 (37%) developed hemodynamic instability during hospitalization (on average, 90 h +/-20 from admission). Troponin I was >0.03 microg/L in 56% of the study population at admission, and predicted occurrence of hemodynamic instability during hospitalization (adjusted hazard ratio 9.8, 95% confidence interval 1.2-79.2), independent to age, gender, co-morbidity, systolic blood pressure, CK-MB, echocardiographic right ventricular dysfunction and other covariates. Twelve patients died during hospitalization (mean time to event 107 h +/-24 from admission); troponin I >0.03 microg/L predicted mortality in univariate analysis, but not after accounting for age, sex and clinical variables. Nevertheless, higher troponin as continuous variable correlated with higher likelihood of in-hospital death (adjusted likelihood ratio 2.2/microg/L, 95% confidence interval 1.1-4.3) in multivariate analysis. In a further multivariate model, CK-MB predicted mortality independent of covariates and troponin I. CONCLUSIONS: In patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I >0.03 microg/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data.