The effects of carvedilol (an alpha.beta-blocker) on lipid metabolism were assessed in addition to its hypotensive effect. The subjects were 18 men and 18 women, 20 with hypertension and 16 normotensives with other conditions requiring carvedilol treatment. They were aged from 31 to 79 years and were given a daily dose of 5-20 mg carvedilol (average, 9.7 mg/day) for 12 weeks. Significant falls were seen in blood pressure and heart rate after 12 weeks in the hypertensive subjects (mean +/- SE) (systolic: from 164 +/- 2 to 141 +/- 2 mm Hg, P less than 0.001; diastolic: from 98 +/- 1 to 85 +/- 2 mm Hg, P less than 0.001; heart rate: from 71 to 65 beats/min, P less than 0.001). Smaller changes in blood pressure and heart rate were seen in the normotensive subjects, with the fall in systolic pressure being significant (from 143 +/- 3 to 135 +/- 2 mm Hg, P less than 0.01). There were no significant changes in the overall serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, and phospholipid levels. In the subgroup with a pretreatment serum triglyceride level of greater than 150 mg/dl, a significant fall of 52.1 mg/dl was seen (P less than 0.05). Lipoprotein analysis showed a significant fall in alpha-lipoprotein levels (P less than 0.05). The atherogenic index did not change significantly, and it was concluded that carvedilol was an effective antihypertensive agent that produced no adverse effects and possibly had beneficial effects on lipid metabolism.

SUMMARY Hypothermic synchronized retroperfusion (HSRP) was applied in closed-chest dogs after acute coronary occlusion to determine whether this intervention can significantly retard the otherwise rapidly developing irreversible ischemic injury. The left anterior descending coronary artery (LAD) was occluded for 3 hours in 22 dogs and for 6 hours in 16 dogs. Starting 30 minutes after occlusion, HSRP was applied during maintained coronary occlusion in 21 dogs. The remaining dogs served as untreated controls. Arterial blood was cooled to 20°C and retroperfused in diastole into the regional coronary veins. Hemodynamics, contrast cineangiography and two-dimensional echocardiography were measured sequentially. Glycogen-depleted ischemic areas and necrotic zones were delineated in transverse slices of the left ventricle.Untreated control dogs further deteriorated; in contrast, HSRP between 30 minutes and 3-or 6-hour LAD occlusion significantly reduced the rate-pressure product (21.3 ± 4.0% or 26.8 ± 8.2%) and left ventricular end-diastolic pressure (39.5 ± 9.5% or 51.4 ± 7.7%) and increased ejection fraction (28 ± 17% and 33 ± 2.0%). HSRP caused no arrhythmias and led to much less necrosis of ischemic myocardium in the treated 3-or 6-hour occlusion series (7.4 ± 2.7% or 28.9 ± 12.6%) than in respective untreated controls (47.1 ± 8.9% and 72.3 ± 5.9%).Moderately hypothermic closed-chest phased retroperfusion appears to protect reversibly injured ischemic myocardium and improve cardiac function. Such treatment may be particularly suitable in the earliest stages of evolving myocardial infarction, when maintenance of myocardial viability is essential for preservation of jeopardized myocardium while awaiting coronary bypass revascularization or nonsurgical thrombolytic reperfusion.

No abstract

No abstract

A 60-year-old manwas diagnosed as adult T-cell leukemia with severe hypercalcemia because of production of parathyroid hormone-related protein. After admission, the patient had respiratory insufficiency with an infiltrative shadow in his lungs suggestive of pneumonia. However, neither improvement in respiratory function nor disappearance of the abnormal chest shadowwas observed with administration of various antibiotics. Anautopsy demonstrated the chest shadow had been caused by metastatic calcification associated with hypercalcemia due to production of parathyroid hormone-related protein. The possibility of metastatic calcification should be considered in patients with adult T-cell leukemia and hypercalcemia who have an abnormal chest shadow. (Internal Medicine 40: 409-413, 2001)