Mechanism of the interaction of hypertension and hypercholesterolemia in atherogenesis: The effects of antihypertensive agents

Any alteration in the balance between serum lipids, platelets, hemodynamic factors, and the blood vessel wall may lead to the development of atherosclerosis. Hypertension and hypercholesterolemia are two major risk factors that accelerate the development of coronary heart disease. The mechanisms of the interactions of these two risk factors are examined in this paper. First, hypertension may be associated with focal or generalized endothelial injury or dysfunction. The altered endothelial functional integrity may predispose to platelet aggregation and altered vessel wall interaction, which may stimulate proliferation and growth of vascular cells. Second, elevated serum cholesterol levels may accelerate lipid deposition and formation of atherosclerotic plaques. In hypertension the rate of clearance of lipoprotein from the vessel wall may be reduced. Third, the sympathetic nervous system may be involved in both the development of hypertension and the alterations of lipid metabolism. Adrenergic activation, which increases blood pressure may also adversely affect lipid metabolism. This is in part α₁-adrenoceptor mediated. Selective α₁-inhibitors have been found to prevent or reduce atherosclerosis in experimental animals. Selective α₁-inhibitors may act at a number of sites on lipoprotein metabolic pathways to favorably influence serum lipids. Taken together, the relationship between hypertension and atherosclerosis involves complex mechanisms. A complete understanding of the mechanisms is of obvious importance.     

急性缺血性脑卒中患者尿微量白蛋白与高血压、糖尿病的关系研究

目的观察急性缺血性脑卒中(AIS)患者尿微量白蛋白与高血压、糖尿病的关系。方法选取103例急性缺血性脑卒中患者,分为高血压与非高血压组、糖尿病与非糖尿病组、同时合并高血压及糖尿病和同时不合并高血压及糖尿病组,各组间进行尿微量白蛋白(MA)的阳性率比较。结果合并高血压组患者MA的阳性率为42.05%,无高血压组患者MA的阳性率为40%,差异无显著性意义(P>0.05);合并糖尿病组患者MA的阳性率为50%,无糖尿病组患者MA的阳性率为33.33%,差异无显著性意义(P>0.05);同时合并高血压、糖尿病组患者MA的阳性率为46.5%,无高血压及糖尿病组患者MA的阳性率为16.67%,差异无显著性意义(P>0.05)。结论MA可能是独立于高血压、糖尿病的急性缺血性脑卒中(AIS)危险因素。     

The effect of diabetic control on very low-density lipoprotein--triglyceride metabolism in patients with type II diabetes mellitus and marked hypertriglyceridemia

We examined the effect of diabetic control on very low-density lipoprotein-triglyceride (VLDL-TG) metabolism in six patients with type II (noninsulin-dependent) diabetes mellitus and marked hypertriglyceridemia. VLDL-TG transport was determined using 3H-glycerol as an endogenous precursor of VLDL-TG, and the resultant kinetic data were evaluated by multicompartmental analysis. Studies were performed in the hypertriglyceridemic diabetic subjects during poor diabetic control and again after 3 months of diabetic treatment, and the results were compared to studies in nondiabetic normolipidemic subjects and nondiabetic subjects with familial forms of hypertriglyceridemia. In the poorly controlled diabetics, mean VLDL-TG synthesis was threefold higher than in the normolipidemic subjects, and the mean fractional catabolic rate (FCR) of VLDL-TG was only one-third of the normals. With diabetic treatment, plasma triglyceride levels fell by more than 50%, but remained fourfold higher than the normals. This was associated with a decrease in mean VLDL-TG synthesis to a level similar to that observed in the genetic hyperlipidemic subjects, but still 2.6-fold higher than the normals. In addition, the mean FCR rose after diabetic control to a level slightly above that of the genetic hyperlipidemic subjects, but remained less than one-half of the normal value. However, the response of VLDL-TG kinetics to diabetic treatment was not uniform. In four subjects, control of hyperglycemia ameliorated the hypertriglyceridemia primarily by decreasing VLDL-TG overproduction. In the other two subjects, diabetic treatment had a greater effect on the FCR than an overproduction of VLDL-TG. Thus, in this select group of diabetic, hypertriglyceridemic subjects, poor diabetic control contributed to both VLDL-TG overproduction and low FCRs. Failure of diabetic treatment to restore VLDL-TG kinetic parameters to normal suggests that the hypertriglyceridemia was due not only to diabetes mellitus but also to an additional abnormality affecting lipoprotein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Management of infections in hospital employees

Hospital employees are often exposed to infectious diseases, both within and outside of the hospital. Susceptible personnel are at risk of acquiring infection and are a possible source of infection for patients, other employees and members of their households. In recent years epidemics in hospitals due to rubella, pertussis, hepatitis B and Legionnaires' disease have included infection transmitted to and from personnel. A comprehensive plan for management of hospital personnel exposed to communicable diseases should include the following: (1) protocols for the management of each of the common infectious diseases; (2) protocols for employees who are at special risk (pregnant women) and employees who work in areas of risk for certain infectious diseases (newborn nursery, clinical and pathology laboratories, hemodialysis unit); (3) assessment of infectious disease experience of new employees by history, skin test (tuberculosis) and serology (rubella, hepatitis B), and a plan for subsequent tests during employment; (4) continuous program of education of employees in infection control; and (5) coordination of policies among administration, employee health service and infection control officer and committee.     

Tensions between academic cardiology and internal medicine

The great number of open heart operations now performed via the right atrium, makes knowledge of the arrangement of the atrial arteries, particularly the sinus node artery, every important for the surgeon. Although studied by anatomists, little attention has been paid to the surgical significance of these arteries. We have therefore examined the distribution of the right atrial arteries and the course of the sinus node artery in 50 normal adult hearts by classic dissection following, in 30 cases, postmortem angiographic studies. Two major arteries of the right atrium were found to be nearly constant. The anterior artery was present in 96% of the cases and supplied the sinus node artery in 32 cases. Of most surgical significance was the lateral artery found in 90% of the cases. This lateral artery was the principal artery to the free atrial wall and in one case gave rise to the sinus node artery.The well-established preponderance of origin of the sinus node artery from the right coronary system (66%) as opposed to the left (30%) was confirmed. Infrequently, a double supply (4%) was seen. Variability was found in the course of the nodal artery relative to the cavoatrial junction — precaval (58%), retrocaval (36%) or encircling (6%).These variations place the atrial arteries in danger when using a right or left atriotomy. The surgeon must be aware of these arteries in order to achieve the safest access to the atrial chambers prior to intracardiac procedures.     

Efficacy of nifedipine therapy for refractory angina pectoris

Nifedipine is a calcium-channel blocking agent that has been effective for patients with angina pectoris when used as single-agent therapy and as part of a combination regimen with conventional antianginal therapy. However, the efficacy of nifedipine in patients with angina refractory to maximum tolerated conventional therapy has not been extensively studied. We present experience using nifedipine in the treatment of three distinct subsets of patients with refractory angina pectoris. One hundred twenty-seven patients with Prinzmetal's variant angina and documented coronary vasospasm were treated with nifedipine after experiencing an inadequate response to conventional therapy. Nifedipine, 40 to 160 mg daily, reduced the mean weekly rate of angina attacks from 16 to 2 (p < 0.001). In 63% of the patients complete control of angina attacks was achieved, and in 87% the frequency of angina was reduced by at least 50%. Nifedipine therapy was well tolerated, and the beneficial response persisted for the 9 months of follow-up. Nifedipine therapy was added to a second group of 11 consecutive patients with refractory episodes of recurrent rest ischemia following acute myocardial infarction. Prior to infarction all the patients had a history of exertional angina only; yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta blockers and/or nitrate preparations. With maximum tolerated conventional therapy the heart rate was lowered to a mean of 65 beats/min and the blood pressure to a mean of $\text{109}\text{70}\text{mm Hg}$. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40 to 120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although resting pains were abolished, and they underwent coronary bypass surgery for rellef of exertional pain. Only one patient continued to have episodes of ischemia at rest, and bypass surgery was necessary for pain relief. The other eight patients have been managed medically for a mean of 5.4 months and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. The third group of patients treated with nifedipine is composed of 239 patients with severe classic exertional angina pectoris without a suspicion of superimposed coronary vasospasm. The anginal episodes in these patients were refractory to maximum tolerated conventional therapy; however, the addition of nifedipine (mean daily dose 60 mg, range 40 to 120 mg) reduced the mean weekly angina attack rate from 20.8 to 6.4 (p < 0.00001). Although only 11% of patients had complete prevention of angina during nifedipine therapy, a total of 70% experienced a reduction in angina frequency of at least 50%. We conclude that the addition of nifedipine therapy may provide further benefit for patients with angina pectoris refractory to maximum tolerated conventional therapy. Randomized, placebo-controlled studies are necessary to confirm the efficacy of nifedipine therapy in patients with refractory angina and to clarify the mechanism of the beneficial response.     

Impaired catabolism of very low-density lipoprotein-triglyceride in a family with primary hypertriglyceridemia

In this report, kinetic studies of plasma very low-density lipoprotein-triglyceride (VLDL-TG) were examined in five brothers (three affected and two unaffected) from a family with primary hypertriglyceridemia. Synthesis and catabolism of VLDL-TG were studied by in vivo labelling of plasma TG with 3H-glycerol, and multicompartmental analysis of the plasma die-away curves. Results of the kinetic studies revealed the following information: (1) one brother, who had the highest plasma TG level and was obese, had both overproduction and a reduced fractional catabolic rate (FCR) of VLDL-TG; (2) second brother, who had moderate hypertriglyceridemia, had a low FCR and high-normal synthesis of VLDL-TG; (3) a third, who had only mildly elevated TG, had a low FCR and normal synthesis of VLDL-TG; and (4) the two normolipidemic brothers had neither overproduction nor decreased FCR of VLDL-TG. The composition of the soluble apoproteins of VLDL was normal. The apoprotein E phenotypes were E4/3 in four brothers, and E3/2 in the fifth. We have reached the following conclusions regarding this family: (1) the common kinetic abnormality of VLDL-TG metabolism in the hypertriglyceridemic brothers was a low clearance of VLDL-TG; (2) impaired catabolism of VLDL could not be explained by the apoprotein C or E patterns; and (3) the most severe hypertriglyceridemia occurred when the decreased FCR was present in conjunction with VLDL-TG overproduction due to obesity. Thus, a moderate defect in catabolism of plasma TG appears to be responsible for one familial form of primary hypertriglyceridemia.