Massive tumorous pulmonary embolism in hepatocarcinoma

Tumoral pulmonary embolism is among the causes of acute dyspnea in patients with neoplasia. This phenomenon, different to thrombotic embolism, occurs frequently in patients with lung, gastrointestinal, liver, breast and uterus neoplasia. It is usually asymptomatic and usually constitutes an autopsy finding in these patients. More rarely it manifests as a cor pulmonale which evolves subacutely. Exceptionally large tumoral emboli spread from a primary tumoral mass, and obstruct main pulmonary arterial vessels, causing a clinical picture indistinguishable from massive pulmonary thromboembolism. We present case of massive tumoral pulmonary embolism by an hepatocarcinoma. In spite of an early thrombolytic treatment the patient died from acute pulmonary hypertension.     

Angiographic evaluation of chronic pulmonary embolism

In some patients acute pulmonary emboli may fail to resolve normally, resulting in chronic pulmonary embolism. This may lead to pulmonary hypertension, respiratory insufficiency, cor pulmonale, and death. The angiographic evaluation in nine patients with chronic pulmonary embolism who underwent embolectomy is presented. Particular emphasis on the predictive value of selective bronchial arteriography in four of these patients is considered. In chronic pulmonary embolism, pulmonary arteries distal to obstructed areas may remain patent and be supplied by hypertrophied bronchial arteries. Since back-bleeding of arterial blood from the bronchial circulation at surgery may predict the success of embolectomy, preoperative bronchial arteriography may be useful for predicting potential surgical success.     

Paradoxic pulmonary vasoconstriction in response to acetylcholine in patients with primary pulmonary hypertension

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.     

Clinical primary pulmonary hypertension: three pathologic types

Clinically, there is a group of patients with elevated pulmonary arterial pressure in whom the underlying cause is not apparent. The pulmonary arterial wedge pressure is not elevated. For such cases, the designation of primary pulmonary hypertension may be made clinically. From the clinical categorization of primary pulmonary hypertension, three distinct pathologic entities emerge, namely 1) plexogenic pulmonary arteriopathy, 2) recurrent pulmonary thromboembolism, and 3) pulmonary veno-occlusive disease. The plexogenic type is characterized initially by pulmonary arterial vasoconstriction with medial hypertrophy. Secondary proliferative intimal lesions, including the plexiform lesion, develop. Recurrent pulmonary thromboembolism is characterized by the presence of arterial thrombi of varying ages involving the microscopic-sized pulmonary arteries. Thrombi may be embolic in nature or may develop in situ. Pulmonary veno-occlusive disease is characterized by obstructive lesions of pulmonary veins and venules. The clinical presentation of the three pathologic types may be so similar that definitive diagnosis depends upon histologic examination of the lung from tissue obtained either by biopsy or at necropsy.     

Intravenous nitroglycerin in acute respiratory failure of patients with chronic obstructive lung disease, secondary pulmonary hypertension and cor pulmonale

We have studied the hemodynamic effects of an intravenous single dose of nitroglycerin in 13 patients with secondary pulmonary hypertension and Cor Pulmonale, during the acute course of respiratory failure and under assisted ventilation. We observed a significant decrease in systolic, diastolic and mean pulmonary arterial pressures, and in pulmonary resistance and systolic right ventricular work index, without any change in right or left pre-loads. The systolic arterial pressure decreased slightly, without any change in cardiac index or diastolic pressure. The arterial and mixed venous oxygen contents, and the pulmonary shunting ( Qs/Qt) were unchanged. These results suggest that nitroglycerin may be a useful therapy in patients in the acute stages of pulmonary hypertension resulting from chronic lung disease and under assisted ventilation. In addition, the lack of change in cardiac index, intrapulmonary shunting and oxygen content suggests that this decrease in pulmonary resistance is not linked with any deleterious effect in oxygen transfer.     

Thoracic aortic dissection that wasn't: CT demonstration of probable paradoxical embolus secondary to unsuspected pulmonary embolus

A patient presented with chest pain, cyanosis and acute ischaemia of the left arm. Aortic dissection was considered to be the likely diagnosis. CT demonstrated multiple large pulmonary emboli and a serpiginous thrombus occluding the origin of the left subclavian artery. Venous thrombosis was proven. The sudden onset of cyanosis followed immediately by a systemic arterial embolus with morphology typical of a venous source was very likely the result of transforaminal shunting induced by massive pulmonary emboli. Post-mortem studies have demonstrated a high incidence of asymptomatic patent foramen ovale in normal individuals. Using contrast echocardiography techniques, any physiological or pathological rise in right heart pressure increases the likelihood of right to left transforaminal shunting of blood or embolic material.     

Recognition and management of pulmonary hypertension

Pulmonary hypertension (mean pulmonary arterial pressure > 20mm Hg at rest or > 30mm Hg during exercise) occurs (i) as primary pulmonary hypertension (no known underlying cause), (ii) as persistent pulmonary hypertension of the newborn or (iii) secondary to a variety of lung and cardiovascular diseases. In the last 10 to 15 years there have been significant advances in the medical management of this debilitating and life-threatening disorder. The main drugs in current use are anticoagulants (warfarin, heparin) and vasodilators, especially oral calcium antagonists, intravenous prostacyclin (prostaglandin I2; epoprostenol) and inhaled nitric oxide. Calcium antagonists, (e.g. nifedipine, diltiazem) are used chiefly in primary pulmonary hypertension. They are effective in patients who give a pulmonary vasodilator response to an acute challenge with a short acting vasodilator (e.g. prostacyclin, nitric oxide or adenosine), and are used in doses greater than are usual in the treatment of other cardiovascular disorders. Prostacyclin, given by continuous intravenous infusion, is effective in patients even if they do not respond to an acute vasodilator challenge. The long term benefit in these patients is thought to reflect the antiproliferative effects of the drug and/or its ability to inhibit platelet aggregation. It is used either as long term therapy or as a bridge to transplantation. Inhaled nitric oxide, which is used mainly in persistent pulmonary hypertension of the newborn, has the particular benefit of being pulmonary selective, due to its route of administration and rapid inactivation. Anticoagulants have a specific role in the treatment of pulmonary thromboembolic pulmonary hypertension and are also used routinely in patients with primary pulmonary hypertension. Nondrug treatments for pulmonary hypertension include (i) supplemental oxygen (> or = 15 h/day), which is the primary therapy in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease and (ii) heart-lung or lung transplantation, which nowadays is regarded as a last resort. Different types of pulmonary hypertension require different treatment strategies. Future advances in the treatment of pulmonary hypertension may come from the use of drug combinations, the development of new drugs, such as endothelin antagonists, nitric oxide donors and potassium channel openers, or the application of gene therapy.     

Minoxidil reduces pulmonary vascular resistance in dogs and cattle

Minoxidil has a direct dilator effect on the systemic arterial smooth muscle. It is potentially an important drug in the treatment of systemic hypertension, especially when combined with beta blockade, which is used to control the associated tachycardia and increase in cardiac output. However, recent observations have suggested that minoxidil might cause pulmonary hypertension. Consequently, we examined the acute effect of monoxidil and propranolol, separately and in combination, on the pulmonary vasculature of the anesthetized dog and the awake calf during normoxia and hypoxia. In both species minoxidil reduced pulmonary vascular resistance. In the dogs this appeared to be the result of a direct action on the pulmonary vascular smooth muscle and in the cattle it was secondary to beta-receptor stimulation. Propranolol alone in the cattle increased the pulmonary pressor response to hypoxia. While we have not examined the possibility that chronic administration of minoxidil might cause pulmonary hypertension by some other mechanism, our acute studies suggest that it reduces, rather than increases, pulmonary vascular resistance. Furthermore, there seems to be a species difference in the mode of its action in dogs and cattle.     

Multidisciplinary treatment of chronic pulmonary insufficiency. 4. The influence of intrathoracic pressure variations on increases in pulmonary vascular pressure during exercise in patients with chronic obstructive pulmonary disease

In the present era of direct monitoring of pressure in patients with chronic obstructive pulmonary disease (COPD), an appreciation of all factors that may influence the observed pulmonary vascular pressures is essential. Our study examines the impact of respiratory variations in intrathoracic pressure on the recorded pulmonary vascular pressures in 28 patients with COPD. Althouth pulmonary hypertension was present in only nine subjects at rest, all had an abnormal increase in the mean pulmonary arterial pressure during supine exercise. In 15 subjects, this abnormal response was, in part, related to an increase in pulmonary arterial wedge pressure to 15 mm Hg or more. The increase in pulmonary arterial wedge pressure was directly related to the amplitude of the peak-to-peak respiratory variation of such wedge pressure. This variation correlated with the specific airway resistance but was not related to the arterial oxygen pressure or pulmonary vascular resistance. These findings indicate the important influence of exaggerated respiratory effort on the measurement of pulmonary arterial wedge pressure and mean pulmonary arterial pressure in patients with chronic obstructive pulmonary disease.     

Aerosolization of novel nitric oxide donors selectively reduce pulmonary hypertension

OBJECTIVES: Inhaled nitric oxide (NO) reduces pulmonary hypertension in acute respiratory failure. Soluble nitric oxide donors (NO/nucleophile adducts-NONOates) are less cumbersome to deliver and may offer clinical advantage compared with inhaled NO. The objective of this study was to examine the pulmonary and systemic hemodynamic effects of tracheal aerosolization of a new class of NONOates in a porcine model of experimentally induced pulmonary hypertension. DESIGN: Prospective, randomized, controlled study. SETTING: Research laboratory. SUBJECTS: Yorkshire pigs (n = 18), weighing 11.4 to 16.4 kg. INTERVENTIONS: In anesthetized, mechanically ventilated, instrumented pigs, steady-state pulmonary hypertension (SSPH) was induced using a thromboxane agonist (U46619). Control animals received tracheal aerosolization of saline (n = 6); EP/NO animals received tracheal aerosolization of ethylputreanine NONOate (EP/ NO, n = 6); and DMAEP/NO animals received aerosolized 2-(dimethylamino) ethylputreanine NONOate (DMAEP/NO, n = 6). MEASUREMENTS AND MAIN RESULTS: Mean pulmonary (MPAP) and mean systemic arterial pressures (MAP), atrial pressures, cardiac output, and arterial blood gases were measured following drug instillation. DMAEP/NO animals had significant reductions in pulmonary vascular resistance index (PVRI) and MPAP at all time points compared with SSPH and control animals (p < .05), while systemic vascular resistance index did not change. EP/NO animals had a significant reduction in PVRI and MPAP at some time points compared with SSPH and control animals. For both NONOate-treated animal groups, MAP and cardiac index did not change significantly compared with SSPH and control animals (p < .05). CONCLUSIONS: In this porcine model of pulmonary hypertension, intratracheal aerosolization of soluble NO donors results in sustained reduction of pulmonary hypertension without reducing systemic arterial pressure. Intermittent aerosolization of NONOates may be an alternative to continuously inhaled NO in the treatment of acute pulmonary hypertension.     

Nitric oxide inhalation: effects on the ovine neonatal pulmonary and systemic circulations

Others have shown that inhaled nitric oxide causes reversal of pulmonary hypertension in anaesthetized perinatal sheep. The present study examined haemodynamic responses to inhaled NO in the normal and constricted pulmonary circulation of unanaesthetized newborn lambs. Three experiments were conducted on each of 7 lambs. First, to determine a minimum concentration of NO which could reverse acute pulmonary hypertension caused by infusion of the thromboxame mimic U46619, the haemodynamic effects of 5 different doses of inhaled NO were examined. Second, the effects of inhaling 80 ppm NO during hypoxic pulmonary vasoconstriction were examined. Finally, to determine if tachyphalaxis occurs during NO inhalation, lambs were exposed to 80 ppm NO for 3 h during which time pulmonary arterial pressure was doubled by infusion of U46619. Breathing NO (80 ppm) caused a slight but significant decrease in pulmonary vascular resistance (PVR) in lambs with normal pulmonary arterial pressure (PAP). Nitric oxide, inhaled at concentrations between 10 and 80 ppm for 6 min (F1O2 = 0.60), caused decreases in PVR when PAP was elevated with U46619. Nitric oxide acted selectively on the pulmonary circulation, i.e. no changes occurred in systemic arterial pressure or any other measured variable. Breathing 80 ppm NO for 6 min reversed hypoxic pulmonary vasoconstriction. In the chronic exposure study, inhaling 80 ppm NO for 3 h completely reversed U46619-induced pulmonary hypertension. Although arterial methaemoglobin increased during the 3-h exposure to 80 ppm NO, there was no indication that this concentration of NO impairs oxygen loading. These data demonstrate that NO, at concentrations as low as 10 ppm, is a potent, rapid-action, and selective pulmonary vasodilator in unanaesthetized newborn lambs with elevated pulmonary tone. Furthermore, these data support the use of inhaled NO for treatment of infants with pulmonary hypertension.     

Chronic thromboembolic pulmonary hypertension

Acute pulmonary hypertension has a high mortality at the onset. Patients surviving the first phase will usually recanalize the pulmonary arteries through intrinsic thrombolytic mechanisms and medical treatment. However, in some cases there is insufficient resolution of the emboli with subsequent thrombotic and fibrotic reorganization, leading to a worsening of the pulmonary obstruction. In the open pulmonary arteries the disease may lead to hypertrophy of the media and intimal proliferation, thus leading to a further increase in the pulmonary vascular resistance. This again leads to hypertrophy of the right ventricle and ultimately to right-sided heart failure. Untreated, chronic thromboembolic pulmonary hypertension has a five-year mortality approaching 100%, but extensive pulmonary thrombendarterectomy using extracorporeal circulation and deep hypothermia has been shown to lower the pulmonary vascular resistance and thereby improve the prognosis significantly. Operative treatment can now be offered in Denmark, and the purpose of this review is to draw attention to the disease, its symptoms, diagnosis and the surgical treatment.     

Flow-dependent pulmonary vasodilation during acute unilateral pulmonary artery occlusion in Jungle Fowl

Giant Jungle Fowl previously were shown to be highly resistant to the onset of pulmonary hypertension syndrome (PHS, ascites) under conditions that induce a substantial incidence of PHS in broiler chickens. In the present study, lightly anesthetized, clinically healthy 12- to 13-wk-old male Giant Jungle Fowl maintained a lower respiratory rate, a similar hematocrit, and superior arterial blood gas values when compared with 6-wk-old male broilers. Giant Jungle Fowl weighed less than broilers (1,860 +/- 19 vs 2,788 +/- 63 g, respectively) and had equivalent absolute values for pulmonary arterial pressure, cardiac output, and pulmonary vascular resistance. Acute unilateral pulmonary artery occlusion in Giant Jungle Fowl doubled the pulmonary vascular resistance and forced the right ventricle to propel a sustained 60% increase in blood flow through the vasculature of the unoccluded lung. A transient increase in pulmonary arterial pressure initially was required to overcome the vascular resistance of the unoccluded lung; however, flow-dependent vasodilation gradually reduced the pulmonary vascular resistance and permitted pulmonary arterial pressure to return toward control levels. Unilateral pulmonary artery occlusion also triggered an immediate reduction in the partial pressure of oxygen in arterial blood, and the gradual return of pulmonary arterial pressure toward control levels did not eliminate this ventilation-perfusion mismatch, which has been attributed to blood flowing too rapidly through the unoccluded lung to permit diffusive gas equilibration. The inherent capacity for flow-dependent pulmonary vasodilation may reduce the susceptibility of Giant Jungle Fowl to PHS by reducing the increment in pulmonary arterial pressure required to propel an elevated blood flow through the lungs.     

Evaluation of pulmonary vascular anatomy and blood flow by magnetic resonance

Rapidly evolving magnetic resonance (MR) imaging techniques provide noninvasive approaches to evaluating morphology and quantitative physiologic information about blood flow in the pulmonary circulation. Important clinical applications currently include the preoperative and postoperative evaluation of congenital abnormalities, assessment of vascular involvement by extrinsic and intrinsic tumors, identification of central thromboemboli, and diagnosis of vascular lung lesions. Ongoing refinements in pulmonary MR angiography may make it possible to use the technique for the noninvasive detection of acute pulmonary emboli in the near future. Quantitative measurements based upon MR flow-encoding sequences are promising for the evaluation of patients with abnormal degrees or distributions of pulmonary blood flow, for example, those with unilateral lung transplants or pulmonary arterial stenoses. MR contrast agents currently under development also show promise for quantitative measurements of regional pulmonary ventilation and perfusion. The coupling of high-resolution anatomic and functional images renders MR a uniquely attractive and powerful method for evaluating the pulmonary vasculature.     

Fragmentation of massive pulmonary embolism using a pigtail rotation catheter

STUDY OBJECTIVES: The purpose of this study was the evaluation of the efficacy and safety of mechanical fragmentation of acute massive pulmonary emboli with a rotatable pigtail catheter. MATERIAL AND METHODS: Ten patients (4 female, 6 male, age 53.8+/-9.5 years) with acute massive pulmonary embolism with hemodynamic impairment were included in the study. The fragmentation catheter device (William Cook Europe A/S; Bjaerverskov, Denmark) consisted of a 5F catheter embedded in a flexible 5.5F sheath. Pulmonary emboli were fragmented by mechanical action of the recoiled rotating pigtail, while the guide wire was exiting an oval side hole proximal to the pigtail tip. In eight cases, an additional thrombolysis was performed. RESULTS: Fragmentation was successful in 7 of 10 patients. Average percentage of recanalization by fragmentation was 29.2+/-14.0%, and 36.0+/-10.0% exclusively of the seven successful cases. Average shock index decreased significantly prefragmentation to postfragmentation from 1.52 to 1.22 (p = 0.03) and to 0.81 48 h later (p < 0.001). Decrease of the average mean arterial pulmonary pressure prefragmentation to postfragmentation was insignificant (from 33 to 31 mm Hg, p = 0.14); further decrease within the 48 h follow-up was highly significant (from 31 to 21 mm Hg, p < 0.001) due to a synergy of fragmentation and thrombolysis (average dose 63+/-25 mg plasminogen activator). There were no procedure-related complications. Overall mortality rate was 20%. CONCLUSION: Fragmentation of massive pulmonary emboli with the pigtail rotation catheter achieved rapid partial recanalization in most cases, with ease of instrumentation, and without complications. Hemodynamic stabilization was completed in synergy with thrombolysis.     

Diagnosis of pulmonary embolism with magnetic resonance angiography

BACKGROUND: Diagnosing pulmonary embolism may be difficult, because there is no reliable noninvasive imaging method. We compared a new noninvasive method, gadolinium-enhanced pulmonary magnetic resonance angiography, with standard pulmonary angiography for diagnosing pulmonary embolism. METHODS: A total of 30 consecutive patients with suspected pulmonary embolism underwent both standard pulmonary angiography and magnetic resonance angiography during the pulmonary arterial phase at the time of an intravenous bolus of gadolinium. All magnetic resonance images were reviewed for the presence or absence of pulmonary emboli by three independent reviewers who were unaware of the findings on standard angiograms. RESULTS: Pulmonary embolism was detected by standard pulmonary angiography in 8 of the 30 patients in whom pulmonary embolism was suspected. All 5 lobar emboli and 16 of 17 segmental emboli identified on standard angiograms were also identified on magnetic resonance images. Two of the three reviewers reported one false positive magnetic resonance angiogram each. As compared with standard pulmonary angiography, the three sets of readings had sensitivities of 100, 87, and 75 percent and specificities of 95, 100, and 95 percent, respectively. The interobserver correlation was good (k=0.57 to 0.83 for all vessels, 0.49 to 1.0 for main and lobar vessels, and 0.40 to 0.81 for segmental vessels). CONCLUSIONS: In this preliminary study, gadolinium-enhanced magnetic resonance angiography of the pulmonary arteries, as compared with conventional pulmonary angiography, had high sensitivity and specificity for the diagnosis of pulmonary embolism. This new technique shows promise as a noninvasive method of diagnosing pulmonary embolism without the need for ionizing radiation or iodinated contrast material.     

Partitioning of pulmonary vascular resistance in primary pulmonary hypertension

OBJECTIVES: This study sought to determine the site of increased pulmonary vascular resistance (PVR) in primary pulmonary hypertension by standard bedside hemodynamic evaluation. BACKGROUND: The measurement of pulmonary vascular pressures at several levels of flow (Q) allows the discrimination between active and passive, flow-dependent changes in mean pulmonary artery pressure (Ppa), and may detect the presence of an increased pulmonary vascular closing pressure. The determination of a capillary pressure (Pc') from the analysis of a Ppa decay curve after balloon occlusion allows the partitioning of PVR in an arterial and a (capillary + venous) segment. These approaches have not been reported in primary pulmonary hypertension. METHODS: Ppa and Pc' were measured at baseline and after an increase in Q induced either by exercise or by an infusion of dobutamine, at a dosage up to 8 microg/kg body weight per min, in 11 patients with primary pulmonary hypertension. Reversibility of pulmonary hypertension was assessed by the inhalation of 20 ppm nitric oxide (NO), and, in 6 patients, by an infusion of prostacyclin. RESULTS: At baseline, Ppa was 52+/-3 mm Hg (mean value+/-SE), Q 2.2+/-0.2 liters/min per m2, and Pc' 29+/-3 mm Hg. Dobutamine did not affect Pc' and allowed the calculation of an averaged extrapolated pressure intercept of Ppa/Q plots of 34 mm Hg. Inhaled NO had no effect. Prostacyclin decreased Pc' and PVR. Exercise increased Pc' to 40+/-3 mm Hg but did not affect PVR. CONCLUSIONS:ns. These findings are compatible with a major increase of resistance and reactivity at the periphery of the pulmonary arterial tree.     

Effect of anatomic distribution of pulmonary emboli on interobserver agreement in the interpretation of pulmonary angiography

OBJECTIVE: This study examines the anatomic distribution of emboli on pulmonary angiography and attempts to determine the relationship of vessel size to interobserver agreement, two factors having important implications in comparing pulmonary angiography with cross-sectional imaging for pulmonary embolism. MATERIALS AND METHODS: One hundred twenty-five consecutive pulmonary angiograms were reviewed retrospectively by three interventional radiologists. Initial interpretations were recorded and compared to determine interobserver agreement on a per-patient and per-embolus basis. Discordant interpretations were reviewed by all radiologists for a consensus interpretation. RESULTS: Unanimous per-patient agreement occurred in 91% (114/125) of initial interpretations. The largest artery containing acute pulmonary embolism was segmental or larger in 24 patients (83% of patients with acute positive findings, 19% of all patients) and subsegmental in only five patients (17% and 4%, respectively). On a per-patient basis, initial interobserver agreement averaged 45% and unanimous consensus agreement was achieved for 79% of patients having isolated subsegmental pulmonary embolism. Consensus readings altered initial per-patient interpretations for 30% of patients having only subsegmental pulmonary embolism; per-embolus interpretations were altered for 37% of all subsegmental emboli. CONCLUSION: Subsegmental emboli occurring as isolated findings are relatively rare. Approximately one third of subsegmental emboli and one third of patients having isolated subsegmental emboli may be initially misdiagnosed on pulmonary angiography. Objections to cross-sectional imaging for pulmonary embolism based on the inability to detect subsegmental pulmonary embolism when compared with pulmonary angiography should be reexamined with this data in mind.     

Paradoxical cerebral embolism during fibrinolysis therapy in deep vein thrombosis and pulmonary embolism

A 37-year-old woman with increasing dyspnoea over several months suddenly developed severe ortho- and tachypnoea as well as cyanosis of the lips and acrocyanosis. Pulmonary angiography revealed massive bilateral pulmonary emboli with a systolic pulmonary artery pressure of 75 mm Hg. Phlebography demonstrated a thrombotic occlusion of the deep veins of the left leg extending to the distal femoral vein. Thrombolysis treatment was started via an indwelling pulmonary artery catheter (500,000 IU urokinase and 10,000 IU heparin as bolus, then 1 mill. IU urokinase and 1,000 IU heparin per hour). After two hours an incomplete left-sided paresis occurred (involving ocular and facial muscles, dysarthria, left arm and left leg) and the thrombolytic infusion was stopped. But cerebral computed tomography (CT) did not demonstrate any intracerebral haemorrhage. The heparin infusion was restarted (partial thromboplastin time between 70 and 90 s). CT examinations during the next few days showed the development of an ischaemic infarction in the distribution of the right medial cerebral artery. Angiography demonstrated occlusion of the right internal carotid artery. The diagnosis of a paradoxical embolus was supported by easy cardiac catheter passage through a patent foramen ovale. Subsequent pulmonary angiography demonstrated a thrombus-free pulmonary arterial circulation with a normal pulmonary arterial pressure. There was gradual and extensive regression of the incomplete hemiparesis.     

Diagnosis, course and prognosis of pulmonary arterial hypertension

Pulmonary arterial hypertension (PAHT) is defined by an increase in mean pulmonary artery pressure above 20 mmHg. Its diagnosis is often easy by cardiac echo-Doppler. Hemodynamic investigation is required in non-echogenic patients or in order to define the type of PAHT: pre- or post-capillary. It is important to determine, on the basis of non-invasive clinical and paraclinical (echocardiography) studies, those patients in whom catheterisation is indicated. PAHT may be due to chronic respiratory disease, left heart disorders, congenital heart disease or follow pulmonary embolism. It is sometimes apparently primary. The prognosis of PAHT depends upon its etiology: when PAHT is secondary to heart disease, it reflects worsening of the causative cardiac problem, which must be corrected. PAHT is a prognostic factor in chronic obstructive lung disease. The course is particularly grave in primary PAHT.