Ivan Pacold

Progression of coronary artery disease after percutaneous transluminal coronary angioplasty

Thirty-nine patients underwent coronary arteriography 1 to 20 months (mean 7 months) after percutaneous transluminal coronary angioplasty (PTCA). At the time of the repeat study, 35 patients (90%) had recurrent angina or myocardial infarction, and 4 patients (10%) were asymptomatic. Restenosis, defined as greater than 50% loss of PTCA gained diameter, was found in 19 patients (49%). In addition, 20 patients had new lesions or marked progression of existing lesions (defined as greater than 20% or increasing greater than 20% obstruction in coronary diameter) in the previously normal or mildly diseased coronary segments. The new or progressive lesions occurred both in patients with restenosis at the PTCA site (nine of 19) and in patients without restenosis (11 of 20). New or progressive lesions tended to occur more commonly in the artery on which PTCA was performed (13 of 40) than in the artery that did not have PTCA (10 of 77) (p less than 0.02 by chi 2). In arteries that had PTCA, new or progressive lesions occurred more often in the segment proximal to the angioplasty site (seven of 13 or 54%) than in the peri-PTCA segment (two of 13 or 15%) and in the segments distal to it (four of 13 or 31%), but this observation did not reach statistical significance. No other clinical, angiographic, or PTCA procedure variables affected the occurrence of new or progressive lesions. In patients with recurrent angina or myocardial infarction after PTCA, both restenosis and new or progressive lesions are common. New lesions or marked progression of existing lesions tended to occur in the vessel subjected to PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease

The effects of orally administered indomethacin or placebo on coronary hemodynamics were studied in 23 patients with coronary artery disease. After indomethacin administration the systemic arterial pressure increased by 12 +/- 4% and the myocardial oxygen consumption by 24 +/- 11%. Coronary sinus flow did not change and coronary vascular resistance increased slightly. Oxygen saturation of the arterial blood did not change, but coronary sinus saturation decreased substantially. Hemodynamic values returned to normal 150 minutes after administration of indomethacin. During rapid atrial pacing, coronary sinus flow increased 79 +/- 14% above the rest value when pacing was done before indomethacin administration; only a 56 +/- 12% increase was seen when pacing was repeated after indomethacin. Peak heart rate achieved during atrial pacing, severity of angina and the degree of ST-segment depression were not altered by indomethacin treatment. Orally administered indomethacin has a mild coronary vasoconstrictive effect that does not interfere substantially with the expected increase in myocardial blood flow during rapid atrial pacing. Anginal threshold is not altered by orally administered indomethacin.

The Effect of Including Cystatin C or Creatinine in a Cardiovascular Risk Model for Asymptomatic Individuals The Multi-Ethnic Study of Atherosclerosis

The authors studied the incremental value of adding serum cystatin C or creatinine to the Framingham risk score variables (FRSVs) for the prediction of incident cardiovascular disease (CVD) among 6,653 adults without clinical CVD utilizing the Multi-Ethnic Study of Atherosclerosis (2000-2008). CVD events included coronary heart disease, heart failure, stroke, and peripheral arterial disease. Variables were transformed to yield optimal prediction of 6-year CVD events in sex-stratified models with FRSVs alone, FRSVs + cystatin C, and FRSVs + creatinine. Risk prediction in the 3 models was assessed by using the C statistic, and net reclassification improvement was calculated. The mean ages were 61.9 and 64.6 years for individuals with and without diabetes, respectively. After 6 years of follow-up, 447 (7.2%) CVD events occurred. In the total cohort, no significant change in the C statistic was noted with FRSVs + cystatin C and FRSVs + creatinine compared with FRSVs alone, and net reclassification improvement for CVD risk was extremely small and not significant with the addition of cystatin C or creatinine to FRSVs. Similar findings were noted after stratifying by baseline presence of diabetes. In conclusion, the addition of cystatin C or serum creatinine to FRSVs does not improve CVD risk prediction among adults without clinical CVD.

Effects of low-dose dobutamine on coronary hemodynamics, myocardial metabolism, and anginal threshold in patients with coronary artery disease.

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 +/- 0.45 micrograms/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p less than .001), and myocardial lactate extraction fell from +17.5% to -1.4% (p less than .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min), and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction.

The usefulness of dobutamine in the assessment of the severity of mitral stenosis

Patients with mitral stenosis often require supine exercise in order to increase their heart rate and cardiac output to assess the severity of their valvular obstruction during cardiac catheterization. We substituted dobutamine for exercise in 14 patients with suspected mitral stenosis. The dobutamine infusion was started at 5 micrograms/kg/min and was increased to 10, 15, and 20 micrograms/kg/min every 3 minutes as tolerated. The heart rate increased from 84 +/- 4 to 123 +/- 7 bpm (p less than 0.001), the cardiac index increased from 2.4 +/- 0.2 to 3.4 +/- 0.2 L/min/m2 (p less than 0.001), and the mean pulmonary artery pressure increased from 27 +/- 3 to 30 +/- 2 mm Hg (p less than 0.02). The pulmonary wedge pressure of 19 +/- 2 mm Hg and the mitral valve index of 0.8 +/- 0.1 cm2/m2 remained unchanged, but the left ventricular end-diastolic pressure decreased from 11 +/- 2 to 6 +/- 2 mm Hg (p less than 0.02). The hemodynamic response during the infusion of dobutamine identified a subgroup of patients with more severe mitral stenosis. Thus, the administration of dobutamine is useful in the evaluation of the severity of mitral valve obstruction during catheterization.

Controversies Regarding Lipid Management and Statin Use for Cardiovascular Risk Reduction in Patients With CKD

Adults with chronic kidney disease (CKD) are at heightened risk for dying of cardiovascular disease. Results from randomized clinical trials of statin drugs versus placebo demonstrate that statin drugs or statin plus ezetimibe reduce the absolute risk for coronary heart disease and mortality among adults with non-dialysis-dependent CKD. The Kidney Disease: Improving Global Outcomes 2013 clinical practice guideline for lipid management in CKD recommends that adults 50 years or older with non-dialysis-dependent CKD be treated with a statin or statin plus ezetimibe regardless of low-density lipoprotein cholesterol levels. However, at least 9 guidelines published during the last 5 years address lipid management for primary and secondary prevention of atherosclerotic cardiovascular disease, and not all guidelines address the utility of lipid-lowering therapy in adults with CKD. Because most patients with CKD receive most of their clinical care from non-nephrologists, differences in recommendations for lipid-lowering therapy for cardiovascular disease prevention may negatively affect the clinical care of adults with CKD and cause confusion for both patients and providers. This review addresses the identification and management of lipid levels in patients with CKD and discusses the existing controversies regarding testing and treatment of lipid levels in the CKD population.

The effects of acute hypertriglyceridemia and high levels of free fatty acids on left ventricular function

The effects of acute hypertriglyceridemia and of high levels of free fatty acids on the left ventricular ejection fraction were studied by radionuclide ventriculography in 20 subjects with and without coronary artery disease. An infusion of approximately 125 ml of a 20% fat emulsion over 25 minutes resulted in an increase of plasma triglycerides to the mean of 820 mg/dl and a fall of the left ventricular ejection fraction from the baseline mean of 62% to 58% (p less than 0.05). Ninety minutes after the intravenous administration of 5000 units of heparin, plasma free fatty acids rose to the mean of 4.6 mmol/L and the mean left ventricular ejection fraction increased to 69% (p less than 0.001). The observed changes in blood lipids were not associated with clinical or ECG evidence of myocardial ischemia. We conclude that acute hypertriglyceridemia causes slight depression of left ventricular performance, while high levels of free fatty acids augment it. However, neither hypertriglyceridemia per se nor its rapid conversion to free fatty acids are likely to cause angina in stable patients with coronary artery disease.

The mechanism and significance of ventricularization of intracoronary pressure during coronary angiography

Ventricularization of pressure during coronary angiography has been said to identify the presence of left main coronary artery disease, but the hemodynamic features and the mechanism of this process have not been studied. Twenty consecutive patients with ventricularization were identified prospectively in our laboratory. Four patients had a discrete ostial left main stenosis and 16 patients had stenosis of the entire length of the left main coronary artery. The degree of pressure drop upon cannulation of the diseased left main coronary artery was highly variable; the systolic pressure decreased by 9 to 94 mm Hg, and the diastolic pressure decreased by 6 to 60 mm Hg. The morphology of the ventricularized pressure was distinct. It had a presystolic deflection resembling an a wave. The upstroke of this waveform was slower and the downstroke was steeper than that of the aortic pressure. An identical waveform was observed in dogs after partial occlusion of the left main coronary artery with a balloon-tipped catheter. The waveform of the so-called ventricularized pressure is derived from the aortic pressure, which is altered by its transmission across the left main coronary stenosis. The appearance of ventricularization is an important clue to the presence of left main coronary artery disease.

Effect of acute postinfusion lipemia and free fatty acids on myocardial contractility: Assessment with radionuclide ventriculography

Equilibrium gated radionuclide ventriculography was used to evaluate the effect of intravenous fat-emulsion overload and excess of free fatty acids (FFA) on left ventricular ejection fraction (LVEF) in 20 patients with and without coronary artery disease (CAD). Fifteen of these patients had normal (>50%) baseline LVEF and 5 had low (<50%) baseline LVEF. From 100 to 150 ml of 20% artificial fat emulsion (Liposyn) was infused over 20–25 min. At the end of the infusion, triglyceridemia reached 820±220 mg% and left ventricular ejection fraction decreased from baseline 62±19% (mean±SD) to 58±16% (P<0.05, paired t-test). After completion of Liposyn infusion, 5,000 U of heparin was administered intravenously and monitoring of LVEF was continuod. One and one-half hours following heparin administration, plasma FFA levels reached 3.7+2.0 mmol/l and LVEF rose to 69±19% (P<0.001, paired t-test). Our data indicate that acute intravenous fat overload can suppress and high pathophysiologic levels of FFA can increase LVEF. This effect is more uniform and statistically more reliable in patients with normal LVEF. The study failed to demonstrate any significant difference in the effect of this pharmacologic intervention between patients with and without CAD.