tonic words: acute cor pulmonale; pulmonary embolism; pulmonary infarction; venous thromboembolism; venous thrombosis Abbreviations: DVT = of great depth venous thrombosis; ELISA = enzyme-linked immunosorbent assay; FSP = fibrin split product; P(A-a)[O.

tonic words: acute cor pulmonale; pulmonary embolism; pulmonary infarction; venous thromboembolism; venous thrombosis

Abbreviations: DVT = of great depth venous thrombosis; ELISA = enzyme-linked immunosorbent assay; FSP = fibrin split product; P(A-a)[O.sub.2] = alveolar-arterial oxygen compressing difference; PIOPED = Prospective Investigation of Pulmonary Embolism Diagnosis; SVCT = spiral volumetric CT; TEE = transesophageal echocardiography; V/Q = ventilation/ perfusion; VTE = venous thromboembolism

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Rudolf Virchow, the brilliant 19th hundred years pathologist, was the first to recognize that kindred clots in the pulmonary artery originate as venous thrombi. He stated: "The detachment of larger or smaller fragments from the extremity of the softening thrombus which are carried along by means of the current of blood and driven into unallied vessels. This gives rise to the extremely frequent process on which I have bestowed the name of Embolia." (1)

All discussions of the pathogenesis of discerning venous thrombosis (DVT) begin with Virchow's triad as follows: hypercoagulability; stasis; and injury to the sailing craft wall. (2) If one examines the commonly accepted risk factors for venous thromboembolism (VTE) (34) nearly all fall into undivided or more of these categories, as shown in Table 1

The greatest in quantity important risk factor for VTE is inherited or acquired hypercoagulability. The first three inherited coagulopathies to be discovered (antithrombin III deficiency, (5) protein C deficiency, (6) and protein s deficiency (5)) are uncommon in the general population and are infrequent in patients with VTE (2 to 5%)

However, as shown in Table 2 the five principally recently discovered hypercoagulable states are far more of frequent occurrence in the general population. Hypercoagulable states are now recognized in > 25% of patients with VTE (7) The incidence of hypercoagulable states is equable higher in patients with idiopathic VTE and in patients with periodical VTE. (8)

With time, we will discover additional genetic failings that lead to hypercoagulability, of the like kind that the majority of patients with VTE will be ground to have a hypercoagulable state. The commonly accepted risk factors for VTE (Table 1) act as precipitants of VTE in patients who have an underlying hypercoagulable state. For example, a 1995 inquiry (9) demonstrated that women with inherited clotting foibles have a 9-fold to 19-fold increase in VTE if they use oral contraceptive agents.

If these speculations are correct, the detection of a hypercoagulable state (10-15) could lead to a more focused approach to VTE prophylaxis. Prophylaxis would be directed to those patients with hypercoagulability when they are expos to individual of the precipitants of (ie, risk factors for) VTE as it is as surgery, trauma, cancer, and pregnancy.

level better, it might be possible to utilize gene therapy or other operations to permanently eliminate the hypercoagulable state. If this were to be possible, the incidence of VTE could be decreased markedly, saving thousands of lives, and saving millions of dollars that generally are spent for the diagnosis and treatment of VTE Further review articles upon pulmonary embolism might not be needed

NATURAL HISTORY OF DVT

In a landmark article in 1969 Kakkar et al (16) delineated the natural history of VTE in patients undergoing surgery without prophylaxis. The fibrinogen uptake standard was utilized to detect postoperative DVT in 132 patients. DVT confirmed from venography, occurred in 40 patients (30%) DVT began in the calf in the majority of patients, and thrombi lys spontaneously in 14 of the 40 patients. Of the remaining 26 patients, the thrombi remained in the calf and did not widen into the popliteal or femoral veins in 17 patients. In nine patients, the thrombi enlargeed into the popliteal or femoral veins, and pulmonary embolism occurr in four of these nine patients. These findings were subsequently confirmed from additional studies. We now recognize that the risk of fatal pulmonary embolism is pendent on the risk of calf vein thrombosis. Without treatment, approximately 20 to 25% of calf vein thrombi continue into the popliteal and femoral veins, causing proximal DVT Without treatment, approximately half of patients with proximal DVT bring out pulmonary embolism as shown in Table 3 (17)

NATURAL HISTORY OF PULMONARY EMBOLISM

In a thought from the Dexter Laboratory in 1975 (18) the annual incidence of pulmonary embolism by year in the United States was estimated to be 630000 It estimated that pulmonary embolism is the major cause of 100000 deaths, and contributes to 100000 other deaths in patients with serious coexisting diseases so as heart disease and cancer. (18)

As shown in Figure 1 we estimated that 11% of patients with acute pulmonary embolism die within 1 h and, therefore, do not receive therapy. Of the 563000 patients who survive at least 1 h the diagnosis is established and treatment is initiated in single 29%, Most of these patients (92%) survive. The majority of deaths come to one's mind among the 400,000 patients in whom pulmonary embolism is not diagnosed or treated. Of the 200000 patients who die of pulmonary embolism, merely 13,000 die because of a lack of rejoinder to treatment. The vast majority of patients (187000) die because of a failure of diagnosis.

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