Most patients with coronary artery disease do not have elevated plasma or low density lipoprotein (LDL) cholesterol. To test whether the protein moiety of LDL, LDL B, might be a parameter to identify ischemic heart disease, the plasma cholesterol, triglyceride, LDL cholesterol, and LDL B were measured in 100 consecutive patients undergoing cardiac catheterization. On the basis of coronary angiography, these patients were divided into two groups: group I, 31 patients without, and group II, 59 atients with significant coronary artery disease. Although clolesterol, triglyceride, and LDL cholesterol levels were all significantly higher in group II, discriminant analysis indicated that LDL B concentrations most clearly separated the two groups. In group I (noncoronary), LDL B was 82 ± 22 mg/100 ml, whereas in group II, LDL B was 118 i 22 mg/100 ml. The B protein level in group I was similar to other normal groups studied (35 asymptomatic male physicians, 83± 11 mg/100 ml; 90 normolipidemic medical students, 72 i 17 mg/100 ml). The results therefore indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia. The explanation for the altered LDL composition observed in this group remains to be elucidated.Atherosclerotic coronary artery disease is a major cause of morbidity and mortality in industrialized countries. The importance of plasma levels of certain lipids and lipoproteins in the pathogenesis of atherosclerosis has been supported by a number of epidemiologic and genetic studies. Briefly, increased levels of total plasma cholesterol and the major cholesterolcarrying lipoproteins, low density (/) lipoproteins (LDL), are associated with an increased risk of developing coronary artery disease (1, 2). Whether an elevated level of plasma triglycerides is an independent risk factor for coronary artery disease is controversial; conflicting evidence has been presented in both epidemiological surveys (3, 4) and in studies in kindreds with familial hypertriglyceridemia (5, 6). A low concentration of another lipoprotein, high density (a) lipoproteins (HDL), appears to be a separate risk factor for coronary artery disease (7), whereas high levels of HDL may have a protective effect (8).Many patients who develop coronary artery disease have normal plasma lipid and lipoprotein cholesterol levels. The presence of disease in some of these patients may be related to the effect of other risk factors such as hypertension and cigarette smoking. Nevertheless, the presence of coronary artery disease in a significant number of these patients remains unexplained.A high correlation between total plasma and LDL cholesterol levels has been found, and it has been assumed that the measurement of LDL by determining its cholesterol content provided an accurate assessment of the concentrat...

Reflected pressure waves returning to the ascending aorta are an important contribution to aortic systolic pressure and thus the load on the left ventricle. The effect of glyceryl trinitrate on pressure wave reflections in the ascending aorta was studied using the transmission of arterial pressure between two high fidelity pressure transducers. Glyceryl trinitrate 0.3 mg sublingually reduced systolic arterial pressure by 11 mmHg owing to a reduction of the late systolic pressure peak. Mean arterial pressure fell 2 mmHg, but heart rate and aortic flow did not change. The aortic input impedance was reduced at the first harmonic (control 18.4(4.1); glyceryl trinitrate 10.8(2.4) kPa.s.litre-1; p less than 0.005) but characteristic impedance was not changed (control 12.7(3.8); glyceryl trinitrate 14.2(3.3) kPa.s.litre-1). The first two harmonics of apparent phase velocity were reduced by glyceryl trinitrate (1.05 Hz: control 3314(798); glyceryl trinitrate 1772(495) cm.s-1; p less than 0.01; 2.1 Hz: control 1246(269); glyceryl trinitrate 754(127) cm.s-1; p less than 0.05), yet the foot to foot wave velocity was unchanged (control 688(112); glyceryl trinitrate 726(112) cm.s-1). There was a significant reduction in the amplitude of the global reflection coefficient at 1.05 Hz (control 0.70(0.09); glyceryl trinitrate 0.48(0.08); p less than 0.001) and at 2.1 Hz (control 0.48(0.07); glyceryl trinitrate 0.23(0.06); p less than 0.005) with no significant change in phase. Glyceryl trinitrate reduces cardiac pulsatile load by diminishing the amplitude of wave reflections arriving back in the aorta during systole yet has no effect on aortic compliance or arteriolar resistance. This study demonstrates a method of evaluating the effect of vasoactive drugs on cardiac pulsatile load.

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