Acute pulmonary embolism and chronic thromboembolic pulmonary hypertension: is there a relationship?

The natural course of acute pulmonary embolism depends primarily on whether the embolism has been detected and treated [1-4]. The haemodynamic severity of acute pulmonary embolism largely depends on the previous state of the cardiopuLmonary system in patients without any previous cardiopulmonary di ease [1, 5], the degree of haemodynamic severity (e.g. that of pulmonary hypertension) depends exclusively on the extent of embolic obstruction [1, 4, 6]. Other factors effecting the natural course of acute pulmonary embolism include age of the embolus and spontaneous thrombolytic activity of the patient's pulmonary vasculature endothelium [3]. Fresh thrombi tend to dissipate into pieces on passage through the right ventricle thereby causing minor embolisms. Older organized thrombi pass unaltered into the pulmonary circulation and frequently get stuck on the pulmonary main branch causing obstruction of major pulmonary arteries [3, 5]. Treatment exerts a major effect on thrombosis . Mean mortality (one month) rates of treated and untreated pulmonary embolism are 8 and 30% respectively [1]. The mortality depends on the degree of pulmonary embolism (mean pulmonary pressure :t5 .3 kPa/40 mmHg·1) is 31%. It is as low as 5.6% in treated patients with moderate or mild pulmonary hypertension (mean pulmonary pressure <5.3 kPa/40 mmHg·1) [5, 6]. Thrombi can be removed from the pulmonary vasculature either by fibrinolysis or by fragmentation. Fibrinolytic dissolution of a thromboembolus is accomplished by the fibrinolytic activity of blood and intima of pulmonary arteries. However, there are interindividual variations in the degree of fibrinolytic activity of pulmonary vessels. The treatment of choice of massive pulmonary embolism especially if it is accompanied by cardiogenic shock or hypotension or signs of right heart failure is thrombolytic therapy-streptokinase [7, 8], urokinase [9, 10], or tissue plasminogen activator [11-14]. At present, the method of choice is i.v. administration of streptokinase. While intravenous administration of tissue plasminogen activator results in rapid remission of right ventricular dilatation on the echocardiogram [15], no significant difference in longterm prognosis has yet been demonstrated between patients treated by streptokinase and those receiving costly rt-PA. In the experience reported by SHARMA et al [16], whereas thrombolytic therapy leads to pulmonary pressure normalization within 4 h, no significant decline in pulmonary pressure can be seen after heparin as late as 24 h after its initiation. Regression of thromboembolic pulmonary vascular obstruction thus depends on the type of treatment, with thrombolytic therapy resulting in far more rapid removal of the vascular obstruction than heparin administration [7-11]. Moreover, regression of the vascular obstruction is dependent on the extent of initial obstruction and the interval to institution of therapy. Our experience shows that the sooner the therapy is initiated, the faster is the regression of pulmonary hypertension in acute pulmonary embolism [ 4, 5]. In 1975, DALEN and ALPERT [1] estimated the total annual prevalence of acute pulmonary embolism in the US at 630,000. 11% of patients with acute pulmonary embolism die suddenly (in less than 1 h). In the early 1980s the percentage of well diagnosed (and hence treated) cases of pulmonary embolism (surviving more than 1 h) in the United States was 29%. This attests to an improving diagnostic capability compared with the fifties and sixties when the proportion of correct diagnoses of pulmonary embolism was as low as 10-11% [17]. According to data released by DALEN and ALPERT [1 ], pulmonary embolism is not recognized and, as a result, remains untreated, in 71% of patients. The mortality of these patients averages 30%. The implication is that 280,000 persons survive undetected and untreated acute pulmonary embolism in the US each year. The fate of these patients is not clear. DALEN and ALPERT [1] believe that recurrent thromboembolic attacks and gradual development of pulmonary hypertension can be expected in half of these patients. Patients with detected and properly treated acute pulmonary embolism are highly unlikely to develop chronic thromboembolic pulmonary hypertension [1, 3, 18-20].