Italian heart journal : official journal of the Italian Federation of Cardiology最新文献

The prognosis of acute pulmonary embolism (PE) is mainly related to the clinical presentation and circulatory state of the patient: the therapeutic strategy is consequently different, ranging from an aggressive treatment in patients in life-threatening clinical conditions to a "stabilization" treatment in those hemodynamically stable. Since the majority of PE patients are clinically stable, a well conducted anticoagulant therapy, either with unfractionated or low-molecular-weight heparins together with a vitamin K antagonist, is sufficient to stop thrombus extension, to minimize the risk of recurrent embolism and prevent mortality. In about 15-20% of cases presenting with clinical instability of variable severity, prompt intravenous thrombolysis with a short-acting compound often represents a life-saving treatment and should be the first-line approach. In normotensive patients with right ventricular dysfunction at echocardiography, who represent about 30% of PE patients, the debate regarding the optimal therapy is still open and further studies are required to document a clinically relevant improvement in the benefit-risk ratio of thrombolytic agents over heparin alone: young people, with a very low risk of bleeding and a concomitant reduction of cardiopulmonary reserve might be the best candidates to systemic thrombolysis. In any case such patients should be admitted to an intensive care unit to monitor the clinical status for at least 48-72 hours and detect signs of possible hemodynamic worsening. Mechanical thrombectomy, either percutaneous or surgical, are ancillary procedures and should be reserved to a minority of highly compromised patients who are unable to receive thrombolysis.

Pulmonary arterial hypertension (PAH) is a clinical condition characterized by elevated vascular resistance, associated with a poor prognosis and usually diagnosed in late stage. Echocardiographic assessment of PAH includes early disease detection and functional heart evaluation, in order to introduce a more accurate surveillance at an early stage of the disease and to contribute to prognostic stratification of advanced disease. Detection involves pulmonary artery systolic pressure (PASP) estimation. There is no clear consensus on defining normal distribution, but a PASP of 36 mmHg has been widely assumed as a cut-off value for mild PAH, requiring a more aggressive surveillance to detect further progression. Functional heart evaluation requires an accurate characterization of morphologic and hemodynamic changes, secondary to PAH development, which involves description of dimensional parameters, ventricular interdependency, intracardiac flow patterns, and right ventricular systolic performance. A valid assessment of these issues results in a useful evaluation of cardiac function, supporting clinical context in defining heart failure condition.

The importance of studying the pathophysiological bases and clinical correlates of exercise limitation in patients with pulmonary arterial hypertension (PAH) is well established. Two modes of exercise testing, the 6-min walk test (6MWT) and the cardiopulmonary exercise test (CPET), are currently proposed for diagnostic, therapeutic and prognostic finalities. The 6MWT is inexpensive, feasible and is thought to better reproduce daily life activities and to reliably detect therapeutic benefits. CPET requires the patient's maximal effort and does not provide a reliable quality of life measure. It is, however, highly reproducible and provides remarkable insights into the pathophysiological mechanisms that lead to exercise intolerance. Due to the limited experience accumulated, CPET is not actually advised for the routine assessment and for the overall clinical decision making of PAH patients. In this review we critically address the knowledge currently acquired on these techniques.

The pulmonary hemodynamic consequences of obstructive sleep apneas have been investigated by several groups during the last 30 years. The earlier data have been obtained by measuring the intravascular pulmonary arterial pressure (PAP) and have shown a rise of PAP during apneas, the highest PAP being observed at the end of apneas. Actually, during obstructive apneas the only reliable measurements are those of transmural PAP which increases throughout the apneas, as a consequence of hypoxic vasoconstriction, and decreases after ventilation has resumed. The link between episodic (nighttime) and permanent (daytime) pulmonary hypertension is poorly understood. Recent studies have clearly indicated that daytime hypoxemia, generally due to an associated chronic airflow obstruction, is the major determinant of permanent pulmonary hypertension and cor pulmonale, and that nocturnal hypoxemia is not sufficient per se.

Multidetector computed tomography (MDCT) and magnetic resonance imaging (MRI) have a leading role in the diagnosis and evaluation of pulmonary arterial hypertension. Technical aspects, advantages, limitations and potential contraindications will be considered. MDCT has many advantages: 1) fast examination, 2) good identification of central and peripheral vessels, 3) good characterization of parenchymal findings, and 4) good evaluation of the heart and mediastinal structures. Limitations are: 1) the use of iodinated contrast material, and 2) radiation exposure. MRI allows: 1) cardiac morphological and functional studies, and 2) identification of central pulmonary arteries. Limitations are: 1) long scanning time, 2) poor definition of peripheral arteries, and 3) impossibility of pulmonary evaluation. MDCT and MRI findings allow: 1) quick diagnosis of pulmonary arterial hypertension, 2) differential diagnosis between primary and secondary forms, 3) evaluation of cardiac manifestations, and 4) morphological and functional follow-up studies in surgically treated and untreated patients.

For many years cardiologists were not interested in studying right ventricular function and the role of the right ventricle in heart failure and in other disease states has therefore been largely underestimated. More recently a consensus has grown on the critical role of right ventricular function in patients with advanced congestive heart failure. The estimation of right ventricular function is nowadays warranted in the standard evaluation of patients with heart failure either due to ischemic heart disease or to primary dilated cardiomyopathy, since it is helpful in the clinical assessment and in the prognostic stratification of such patients. Most information may be obtained non-invasively using sound but simple and reproducible echocardiographic indicators of right ventricular function.

A percentage ranging from 0.1 to 4.0 of patients recovering from acute pulmonary embolism develop chronic thromboembolic pulmonary hypertension (CTEPH). Without intervention, CTEPH is a progressive and lethal disease for which there is no effective medical therapy. Pulmonary endarterectomy (PEA) is the treatment of choice. Lung transplantation is indicated only in few cases when PEA is not feasible. Since 1994 at the IRCCS San Matteo Hospital - University of Pavia (Italy), 134 PEAs have been performed. Preoperatively, NYHA class distribution was respectively 3-II, 56-III, and 75-IV; mean pulmonary artery pressure and pulmonary vascular resistances were 47 +/- 13 mmHg and 1149 +/- 535 dynes*s*cm(-5) respectively. The overall operative mortality has been 9.7% (4.5% in 2004). Survival at 3-month, 1-year, and 3-year follow-up was 89.5 +/- 2.6, 87.8 +/- 2.9, and 83.3 +/- 3.5% respectively; this last rate was unchanged up to 10 years. After PEA, mean pulmonary artery pressure and pulmonary vascular resistances were 25 +/- 9 mmHg and 322 +/- 229 dynes*s*cm(-5) respectively and these results were stable over time. At the 3-year follow-up, 94% of patients were in NYHA class I or II and the only therapy is anticoagulation.

In 90% of cases the clinical suspicion of pulmonary embolism (PE) is raised by clinical signs and symptoms, while in only 10% of cases PE is suspected on the basis of electrocardiographic, arterial blood gas analysis or radiological findings. The combination of clinical signs and symptoms and the results of first-level diagnostic tests (electrocardiography, gas analysis and chest X-ray) allows a fairly accurate classification of patients with "clinical suspicion of PE" into three categories of clinical (or pre-test) probability: low, intermediate and high. The clinical diagnosis of PE is very often inaccurate making the use of additional tests, including imaging techniques, mandatory. The choice and the combination (= diagnostic algorithms) of second- and third-level diagnostic tests (D-dimer, venous ultrasound, echocardiography, lung scintigraphy, helical computed tomography and pulmonary angiography) depend primarily on the clinical conditions of patients and their pre-test probability. We propose two diagnostic algorithms: 1) a diagnostic algorithm for patients with clinically suspected PE and critical clinical conditions (unstable patients), 2) a diagnostic algorithm for patients with clinically suspected PE and non-critical clinical conditions (hemodynamically stable patients).

For the majority of patients with pulmonary embolism the recommended therapy consists of a 5 to 7 day treatment with heparin followed by a treatment with oral anticoagulants given for at least 3 months. The currently recommended duration of oral anticoagulant treatment for pulmonary embolism is the result of the balance between the benefit provided by treatment, essentially the prevention of recurrence, and the bleeding risk and inconvenience associated with treatment. Risk of bleeding and inconvenience should be assessed on an individual base. Concerning the risk of recurrence, patients with pulmonary embolism can be classified in three groups: patients with pulmonary embolism associated with temporary risk factors, patients with pulmonary embolism associated with persistent risk factors, patients with pulmonary embolism occurring in the absence of any identifiable temporary or persistent risk factors for venous thromboembolism (idiopathic or unprovoked pulmonary embolism). Due to the limitations of the currently available oral anticoagulant agents, search for the optimal agent to be used in the long-term treatment of pulmonary embolism is still open.

Pulmonary arterial hypertension (PAH) is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance leading to right ventricular failure and premature death. Recently, the diagnostic approach has been more clearly defined according to the new clinical classification and with consensus reached on algorithms of various investigative tests and procedures that exclude other causes and ensure an accurate diagnosis of PAH. The diagnostic procedures include clinical history and physical examination, ECG, chest X-ray, transthoracic Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, ventilation and perfusion lung scan, high-resolution computed tomography of the lungs, contrast-enhanced spiral computed tomography of the lungs and pulmonary angiography, blood tests and immunology, abdominal ultrasound scan, exercise capacity assessment, and hemodynamic evaluation. Invasive and non-invasive markers of disease severity, either biomarkers or physiological parameters and tests that can be widely applied, have been proposed to reliably monitor the clinical course.