PubMed · 14732726
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Feng J He, Graham A MacGregor. 2004-01-19. Universal salt reduction.. https://doi.org/10.1161/01.hyp.0000115923.42167.30
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In this paper, a class of conditional mixed models is proposed to adjust for non-ignorable drop-out, while also accommodating unequal follow-up due to staggered entry and administrative censoring in longitudinal studies. Conditional linear and quadratic models which model subject-specific slopes as linear or quadratic functions of the time-to-drop-out, as well as pattern mixture models are both special cases of this approach. We illustrate these models and compare them with the usual maximum likelihood approach assuming ignorable drop-out using data from a multi-centre randomized clinical trial of renal disease. Simulations under various scenarios where the drop-out mechanism is ignorable and non-ignorable are employed to evaluate the performance of these models.
High blood pressure (BP) ranks as the greatest risk factor for cardiovascular disease. The increased cardiovascular risk determined in recent interventional studies has led the health authorities in some countries to re-ignite the discussion about whether hypertension should be listed as a contraindication for hormone replacement therapy (HRT). We reviewed papers published since 1960 and listed in MEDLINE, EMBASE and Biosis, on studies that monitored the course of BP during HRT. We found that both primarily normotensive and hypertensive postmenopausal women actually run only a very low risk of BP increase during HRT, indeed, BP was often lowered. In one of our own studies 1397 hypertensive women with BP diastolic >95 mmHg received transdermal HRT regimens; BP was lowered by an average of 7 mmHg systolic and 9 mmHg diastolic. The results of the more recent 24-h ambulatory BP studies are particularly conclusive. At least 19 such studies have been performed, 13 placebo-controlled and 10 cross-over; 5 found no effect on BP and 14 studies demonstrated BP reductions. BP was lowered by treatment with transdermal estradiol in 11 of 13 studies and by oral estrogen in 4 of 11 studies. The effects were not consistent with regard to systolic or diastolic BP nor to action on day- and night-time BP. It cannot be ruled out that some women with a particular predisposition exhibit an abnormal reaction to the vasoactive effects of HRT, and there is a paucity of long-term data on risk populations, specifically on the progestogenic effects in patients with pre-existing arteriosclerotic lesions. In conclusion, the risk of developing hypertension during HRT is very low, but hormone therapy should always be appropriately indicated and during therapy BP should be checked regularly.
Although present in many patients with heart failure and a normal ejection fraction, the role of isolated impairments in active myocardial relaxation in the genesis of elevated filling pressures is not well characterized. Because of difficulties in determining the effect of prolonged myocardial relaxation in vivo, we used a cardiovascular simulated computer model. The effect of myocardial relaxation, as assessed by tau (exponential time constant of relaxation), on pulmonary vein pressure (PVP) and left ventricular end-diastolic pressure (LVEDP) was investigated over a wide range of tau values (20-100 ms) and heart rate (60-140 beats/min) while keeping end-diastolic volume constant. Cardiac output was recorded over a wide range of tau and heart rate while keeping PVP constant. The effect of systolic intervals was investigated by changing time to end systole at the same heart rate. At a heart rate of 60 beats/min, increases in tau from a baseline to extreme value of 100 ms cause only a minor increase in PVP of 3 mmHg. In contrast, at 120 beats/min, the same increase in tau increases PVP by 23 mmHg. An increase in filling pressures at high heart rates was attributable to incomplete relaxation. The PVP-LVEDP gradient was not constant and increased with increasing tau and heart rate. Prolonged systolic intervals augmented the effects of tau on PVP. Impaired myocardial relaxation is an important determinant of PVP and cardiac output only during rapid heart rate and especially when combined with prolonged systolic intervals. These findings clarify the role of myocardial relaxation in the pathogenesis of elevated filling pressures characteristic of heart failure.