[A prospective study of oral anticoagulation therapy monitored with the P&P-test.].

OBJECTIVE: To analyze the outcome of patients on oral anticoagulation therapy who are monitored with the prothrombin proconvertin time (P&P-test, PP). MATERIAL AND METHODS: The prothrombin-proconvertin time was used to adjust anticoagulant intensity in a prospective study of 326 patients treated with oral anticoagulants for a study period of 121 patient years. The goal intensity INR was 2.0-3.0 for all patients. The main indications were: artificial heart valves 26%, venousthromboembolism 25%, atrial fibrillation 23%, atherosclerotic disease 14% and systemic arterial embolism of uncertain etiology 7%. RESULTS: INR calculated directly from the PP correlated well with INR calculated from the PT. The mean time adjusted anticoagulant intensity was 2.3 and did not differ significantly according to indication. Six major bleedings, including one fatal, occurred in five patients during the study period. The INR was 1.8 in one patient who bled from a duodenal ulcer, but 6.8,7.9,8.6,11.6 (died) and 15.5 at five other events. The INR was <4.5 during 97% of the treatment time of the whole group and 1% of treat notment time were at an INR>6.0. The bleeders had a different pattern with 18% of the treatment time at INR>6.0. The risk of bleeding was one for every 73 days at that intensity or an almost 600 fold risk increase compared to an INR<4.5. One patient anticoagulated for systemic embolism had cerebral infarction with an event related INR of 2.0. Two patients with atrial fibrillation died from acute myocardial infarction but event related INR's were not available. One patient anticoagulated for venous thromboembolism died suddenly but was not autopsied. No embolic events occurred in patients with artificial heart valves in spite of the low intensity anticoagulation. CONCLUSION: Despite a relatively low intensity in all patient groups in this study thromboembolic events were rare. The risk of bleeding increased markedly at INR>6.0. The mortality rate of the ariticoagulated population was comparable to the expected age adjusted Icelandic mortality rate.

Performance of prothrombin-proconvertin time as a monitoring test of oral anticoagulation therapy.

Outcome and anticoagulation intensity was evaluated during 121 patient years of oral anticoagulant therapy monitored with the prothrombin-proconvertin clotting time (PP, also known as P&P). The PP-based international normalized ratio (INR; PP-INR) correlated well with the INR calculated from the prothrombin clotting time (PT; r = 0.92), and results were almost identical over a wide range after linear conversion (1/INR). When the PP-INR was 4.5 or less, the risk of major bleeding was 1 for every 118 treatment years, but it was 1 for every 73 days when the INR was 6 or more. The 1/PP-INR correlated better with factor II coagulant activity (r = 0.85) than did the 1/PT-INR (r = 0.78). The 1/PP-INR also correlated better with the native prothrombin antigen (r = 0.76) than did the 1/PT-INR (r = 0.68). The PP and PT results correlated better with factor II coagulant activity than with native prothrombin antigen. Thus, the PP clotting time results can be accurately converted to INR. The results also suggest that the PP may have advantages over the PT as an indicator of anticoagulation intensity during oral anticoagulation.

Angiographic predictors of new coronary occlusions.

To determine whether coronary angiography is predictive of the future site of coronary occlusion, we analyzed the coronary angiograms of 246 consecutive patients having two or more angiograms without therapeutic invasive intervention in the interval between angiograms. The average interval between studies was 46 months. Of 2183 normal segments at the first angiogram, 51 (2.3%) were occluded at the second angiogram, whereas in segments with minimal disease (1% to 25% diameter stenosis) 33 (8%) of 411 were occluded (p < 0.05). There was a further stepwise increase in the occlusion ratio, with increasing stenosis reaching a 31% occlusion ratio in lesions with critical (91% to 99%) stenosis at the first angiogram. For any given degree of stenosis, the occlusion ratio of "long" lesions (5 to 20 mm) was on the average more than twice that of "short" lesions (< 5 mm, p < 0.01), except in lesions with critical stenosis (91% to 99%) where length was no longer important. Occlusion of segments judged free of disease on the first angiogram was highest in the right coronary artery, 4.7%, versus 2.7% in the left anterior descending and 0.6% in the circumflex artery (p < 0.01). History of recent myocardial infarction was a good clinical predictor of occlusion and deterioration of ventricular function.

Renovascular hypertension and coronary heart disease complicating essential thrombocythemia.

A 36-year-old male was evaluated for treatment-resistant hypertension. A high platelet count 828 x 10(9).l-1, led to the diagnosis of essential thrombocythemia (ET). Aorto-renal angiography revealed critical bilateral renal artery stenosis and coronary angiography showed three-vessel disease. Percutaneous transluminal renal angioplasty was only partially successful. The patient received a 12-week course of busulphan and subsequently the thrombocyte count decreased to 200 x 10(9).l-1. Renal angiography 12 months later showed bilateral regression of the renal artery stenosis with lowering of the blood pressure to normal levels.

Additive effects of moderate dietary salt reduction and captopril in hypertension.

In a randomized, cross-over study 27 patients had diastolic blood pressure of greater than or equal to 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was less than or equal to 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash-out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 +/- 12/6 mmHg recumbent and 140/91 +/- 11/7 standing, following captopril 144/94 +/- 13/5 and 132/92 +/- 12/6, respectively, with low salt diet added to captopril 140/91 +/- 12/6 and 128/89 +/- 11/6 and with hydrochlorothiazide and captopril 133/86 +/- 12/7 and 120/84 +/- 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.