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Kinetics of apo B and apo AI were assessed in 8 patients with mixed hyperlipidemia at baseline and after 8 weeks of atorvastatin 80 mg q.d. and micronised fenofibrate 200 mg q.d. in a cross-over study. Both increased hepatic production and decreased catabolism of VLDL accounted for elevated cholesterol and triglyceride concentrations at baseline. Atorvastatin significantly decreased triglyceride, total, VLDL and LDL cholesterol and apo B concentrations (−65%, −36%, −57%, −40% and −33%, respectively, P< 0.05). Kinetic analysis revealed that atorvastatin stimulated the catabolism of apo B containing lipoproteins, enhanced the delipidation of VLDL1and decreased VLDL1production. Fenofibrate lowered triglycerides and VLDL cholesterol (−57% and −64%, respectively, P< 0.05) due to enhanced delipidation of VLDL1and VLDL2and increased VLDL1catabolism. Changes of HDL particle composition accounted for the increase of HDL cholesterol during atorvastatin and fenofibrate (18% and 23%, P< 0.01). Only fenofibrate increased apo AI concentrations through enhanced apo AI synthesis (45%, P< 0.05).

Apolipoprotein B (apoB) metabolism was investigated in 20 men with plasma triglyceride 0.66-2.40 mmol/l and plasma cholesterol 3.95-6. 95 mmol/l. Kinetics of VLDL(1) (S(f) 60-400), VLDL(2) (S(f) 20-60), IDL (S(f) 12-20), and LDL (S(f) 0;-12) apoB were analyzed using a trideuterated leucine tracer and a multicompartmental model which allowed input into each fraction. VLDL(1) apoB production varied widely (from 5.4 to 26.6 mg/kg/d) as did VLDL(2) apoB production (from 0.18 to 8.4 mg/kg/d) but the two were not correlated. IDL plus LDL apoB direct production accounted for up to half of total apoB production and was inversely related to plasma triglyceride (r = -0.54, P = 0.009). Percent of direct apoB production into the IDL/LDL density range (r = 0.50, P < 0.02) was positively related to the LDL apoB fractional catabolic rate (FCR). Plasma triglyceride in these subjects was determined principally by VLDL(1) and VLDL(2) apoB fractional transfer rates (FTR), i.e., lipolysis. IDL apoB concentration was regulated mainly by the IDL to LDL FTR (r = -0.71, P < 0.0001). LDL apoB concentration correlated with VLDL(2) apoB production (r = 0.48, P = 0.018) and the LDL FCR (r = -0.77, P < 0. 001) but not with VLDL(1), IDL, or LDL apoB production. Subjects with predominantly small, dense LDL (pattern B) had lower VLDL(1) and VLDL(2) apoB FTRs, higher VLDL(2) apoB production, and a lower LDL apoB FCR than those with large LDL (pattern A). Thus, the metabolic conditions that favored appearance of small, dense LDL were diminished lipolysis of VLDL, resulting in a raised plasma triglyceride above the putative threshold of 1.5 mmol/l, and a prolonged residence time for LDL. This latter condition presumably permitted sufficient time for the processes of lipid exchange and lipolysis to generate small LDL particles.

Four patients had deviation of the mean QRS axis as an electrocardiographic manifestation of hyperkalemia. Two patients had a leftward and superior axis shift and two had a rightward and inferior axis shift. These findings are reported so that the spectrum of electrocardiographic changes associated with hyperkalemia will be appreciated.

EXTERNAL direct-current and alternating-current countershock has proved effective in terminating ventricular tachycardia. Various medications have also been used to control this arrhythmia. This paper describes the successful use of frequent intermittent, intravenous administration of lidocaine (Xylocaine) hydrochloride to control recurrent ventricular tachycardia after the failure of other commonly available drugs. REPORT OF A CASE A 31-year-old white woman was admitted to the hospital for elective pelvic surgery. There was a history of eight normal full-term deliveries, two spontaneous abortions, and dilation and curettage had been done five times. She had had two brief episodes of palpitations, 13 and 9 months previously. Evaluation after the latter episode revealed an innocent cardiac murmur.On this admission a grade II (of VI), basal, systolic ejection murmur was heard and considered to be innocent. Results of urinalysis and serological study were normal, and a hemogram and chest roentgenogram were normal. An electrocardiogram was not

The recognition of coronary artery disease CAD in the asymptomatic, presumably healthy population is an ongoing medical problem. In an attempt to prevent untoward cardiovascular events in individuals who are at a relatively high risk for developing CAD and to modify changeable risks, the United States Army initiated a cardiovascular screening program for all active duty Army personnel over the age of 40 years. Criteria for primary cardiovascular screen failure include any one of the following abnormalities 1 Framingham risk index ≥ 5, 2 abnormal cardiovascular history or examination, 3 abnormal electrocardiogram, and 4 fasting blood sugar ≥ 115 mgdl. Failure of the primary screen requires the taking of a secondary screening test, which includes an internal medicine or cardiology consultation and a maximum symptomlimited exercise treadmill test andor further sequential followup. During the followup, recommendations are made for risk factor modification and exercise programs. Between June 1981 and August 1983, 42,752 individuals have been screened. Of these, 23,428 55 have cleared the primary screen, 7,279 17 have cleared the secondary screen, and 1,040 2.4 have not passed the secondary screen.