Walnuts and endothelial function in hypercholesterolemic subjects.
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Antioxidants↗
Biomedical subjects
Michael Shechter
Publications and source records attributed to Michael Shechter.
Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction.
BACKGROUND: Although clopidogrel reduces the risk of cardiovascular episodes after coronary events and stenting, a substantial number of incidents continue to occur. METHODS AND RESULTS: The antiplatelet effect of clopidogrel was studied prospectively in 60 consecutive patients who underwent primary angioplasty (percutaneous coronary intervention [PCI]) with stenting for acute ST-segment-elevation myocardial infarction (STEMI) to determine whether variability in response to clopidogrel affects clinical outcomes. Patients were stratified into 4 quartiles according to the percentage reduction of ADP-induced platelet aggregation. Although patients in the first quartile were resistant to the effects of clopidogrel (ADP-induced platelet aggregation at day 6, 103+/-8% of baseline), ADP-induced aggregation was reduced to 69+/-3%, 58+/-7%, and 33+/-12% of baseline, respectively, in patients in quartiles 2 through 4 (P<0.01 for all). In addition, epinephrine-induced platelet aggregation and platelet aggregation under flow conditions, assessed by the cone-and-plate(let) analyzer method, were reduced significantly less in the first quartile than in quartiles 2 through 4. Whereas 40% of patients in the first quartile sustained a recurrent cardiovascular event during a 6-month follow-up, only 1 patient (6.7%) in the second quartile and none in the third and fourth quartiles suffered a cardiovascular event (P=0.007). CONCLUSIONS: Up to 25% of STEMI patients undergoing primary PCI with stenting are resistant to clopidogrel and therefore may be at increased risk for recurrent cardiovascular events.
Adenosine Diphosphate↗
Impact of short-term intermittent intravenous dobutamine therapy on endothelial function in patients with severe chronic heart failure.
BACKGROUND: Intermittent intravenous dobutamine therapy is used to treat patients with decompensated end-stage chronic heart failure (CHF), in whom the vascular endothelium is usually impaired. Although it has been suggested that modification or reversal of endothelial dysfunction may be of significant therapeutic benefit, the impact of short-term intermittent intravenous dobutamine therapy on flow-mediated dilation (FMD) in patients with severe decompensated end-stage chronic CHF has not been assessed. METHODS: We prospectively assessed the impact of intermittent intravenous low-dose dobutamine therapy on endothelium-dependent brachial artery FMD and endothelium-independent nitroglycerin (NTG)-mediated vasodilation using high resolution ultrasound scanning in 20 consecutive male patients with severe CHF and ischemic cardiomyopathy (New York Heart Association functional class IV), at baseline and after 4 months, and compared them to 20 age- and sex-matched control subjects. The cardiac index (CI), stroke index (SI), and systemic vascular resistance (SVR) were assessed non-invasively with a thoracic electrical bioimpedance device before and after intravenous dobutamine therapy. RESULTS: Intermittent intravenous dobutamine therapy resulted in significant improvement in post-intervention FMD compared with baseline (7.7% +/- 2.4% vs 1.1% +/- 2.6%; P = .001), a finding not evident in control subjects (1.3% +/- 2.6% vs 1.2% +/- 2.1%; P = .78). There was no significant effect of dobutamine treatment compared with control subjects on NTG-induced vasodilation (7.6% +/- 5.5% vs 7.5% +/- 8.8%, P = .979). Short-term dobutamine therapy also significantly improved SVR (1797 +/- 926 dyne sec/cm5 vs 2172 +/- 1133 dyne sec/cm5, P = .05), CI (2. 4+/- 0.6 L/min/m2 vs 1.9 +/- 0.6 L/min/m2, P = .01), and SI (33.5 +/- 11.7 mL/m(2) vs 27.2 +/- 12.4 mL/m2, P = .02). CONCLUSIONS: Short-term intermittent intravenous low-dose dobutamine therapy significantly improved vascular endothelial function, perhaps demonstrating an additional mechanism for improved SVR, CI, and SI in patients with severe CHF.
Adrenergic beta-Agonists↗
Oral acetylcysteine as an adjunct to saline hydration for the prevention of contrast-induced nephropathy following coronary angiography. A randomized controlled trial and review of the current literature.
AIMS: To determine laboratory and clinical benefit of oral acetylcysteine, as an adjunct to saline hydration, in chronic renal insufficiency patients undergoing coronary angiography. METHODS AND RESULTS: We prospectively studied 80 patients with chronic renal insufficiency (mean [+/-SD] serum creatinine concentration 2.0+/-0.39mg/dl), who underwent coronary angiography with or without intervention. Patients were randomly assigned to receive either acetylcysteine (600mg orally t.i.d.) or placebo, in addition to intravenous 0.45% saline (1ml/kg of body weight per hour), 12h prior to and after coronary angiography. There was an increase of >/=0.5mg/dl in the serum creatinine concentration 48h after coronary angiography in seven of the 80 patients (9%): in four of the 41 patients (10%) in the acetylcysteine group and in three of the 39 patients (8%) in the placebo group (P=0.52). The incidence of in-hospital adverse clinical events (acetylcysteine, 5% vs placebo, 8%, P=0.47) and the length of hospital stay [acetylcysteine, median (interquartile range) 4 (2-4) days vs placebo, 2 (2-4) days, P=0.44] did not differ significantly between the two treatment groups. CONCLUSION: Our findings do not support routine prophylactic administration of oral acetylcysteine as an adjunct to saline hydration for the prevention of contrast-induced nephropathy in chronic renal insufficiency patients undergoing coronary angiography.
Acetylcysteine↗
The assessment of infarct size in postmyocardial infarction patients undergoing thallium-201 tomographic imaging is improved using attenuation correction.
PURPOSE: Attenuation correction (ATC) has been shown to improve the accuracy of thallium-201 single photon emission computed tomography (SPECT) for the detection and evaluation of patients with coronary artery disease. The purpose of this study was to evaluate the value of ATC for the assessment of infarct size in patients after myocardial infarction (MI). MATERIALS AND METHODS: Tl-201 SPECT with ATC was performed on 39 patients with 49 previous MIs. This was followed by radionuclide ventriculography for the assessment of global and regional left ventricular function. Uncorrected and corrected 24-hour redistribution SPECT images were analyzed for regional perfusion using a 5-point segmental scoring scale from 0 (normal) to 4 (absent) thallium uptake. RESULTS: The mean number of segments with scores of >1 and 2 was significantly higher without ATC than with ATC (5.3 +/- 3.6 vs. 3.5 +/- 3.6, P = 0.0001 for scores >1; 3.8 +/- 3.6 vs. 2.5 +/- 3.0, P = 0.0001 for scores of >2, respectively). The mean total number of segments with scores of >1 assessed without ATC was significantly higher compared with that assessed with ATC (16.9 +/- 13.5 vs. 11.2 +/- 12.2, P = 0.0001). Evaluation without ATC demonstrated only a fair correlation between the SPECT parameters (number of segments with scores of >1 and >2, and total score of segments with scores of >1) and left ventricular regional and global function, whereas there was a clear improvement in all the parameters after ATC. With ATC, a decrease in infarct size was demonstrated in 27 of the 49 infarcts (55%). CONCLUSIONS: The improved correlation with left ventricular function indicates that SPECT imaging with ATC provides a more accurate assessment of infarct size in post-MI patients. The use of nonattenuation-corrected SPECT imaging overestimates infarct size in a majority of patients.
Adult↗
External counterpulsation therapy improves endothelial function in patients with refractory angina pectoris.
OBJECTIVES: The goal of this study was to investigate the influence of short-term external counterpulsation (ECP) therapy on flow-mediated dilation (FMD) in patients with coronary artery disease (CAD). BACKGROUND: In patients with CAD, the vascular endothelium is usually impaired and modification or reversal of endothelial dysfunction may significantly enhance treatment. Although ECP therapy reduces angina and improves exercise tolerance in patients with CAD, its short-term effects on FMD in patients with refractory angina pectoris have not yet been described. METHODS: We prospectively assessed endothelial function in 20 consecutive CAD patients (15 males), mean age 68 +/- 11 years, with refractory angina pectoris (Canadian Cardiovascular Society [CCS] angina class III to IV), unsuitable for coronary revascularization, before and after ECP, and compared them with 20 age- and gender-matched controls. Endothelium-dependent brachial artery FMD and endothelium-independent nitroglycerin (NTG)-mediated vasodilation were assessed before and after ECP therapy, using high-resolution ultrasound. RESULTS: External counterpulsation therapy resulted in significant improvement in post-intervention FMD (8.2 +/- 2.1%, p = 0.01), compared with controls (3.1 +/- 2.2%, p = 0.78). There was no significant effect of treatment on NTG-induced vasodilation between ECP and controls (10.7 +/- 2.8% vs. 10.2 +/- 2.4%, p = 0.85). External counterpulsation significantly improved anginal symptoms assessed by reduction in mean sublingual daily nitrate consumption, compared with controls (4.2 +/- 2.7 nitrate tablets vs. 0.4 +/- 0.5 nitrate tablets, p <0.001 and 4.5 +/- 2.3 nitrate tablets vs. 4.4 +/- 2.6 nitrate tablets, p = 0.87, respectively) and in mean CCS angina class compared with controls (3.5 +/- 0.5 vs. 1.9 +/- 0.3, p <0.0001 and 3.3 +/- 0.6 vs. 3.5 +/- 0.5, p = 0.89, respectively). CONCLUSIONS: External counterpulsation significantly improved vascular endothelial function in CAD patients with refractory angina pectoris, thereby suggesting that improved anginal symptoms may be the result of such a mechanism.
Aged↗
Atorvastatin and the ability of clopidogrel to inhibit platelet aggregation.
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Atorvastatin↗
Effects of oral magnesium therapy on exercise tolerance, exercise-induced chest pain, and quality of life in patients with coronary artery disease.
Previous studies have demonstrated that magnesium supplementation improves endothelial function in patients with coronary artery disease (CAD). However, the impact on clinical outcomes, such as exercise-induced chest pain, exercise tolerance, and quality of life, has not been established. In a multicenter, multinational, prospective, randomized, double-blind and placebo-controlled trial, 187 patients with CAD (151 men, 36 women; mean +/- SD age 63 +/- 10 years, range 42 to 83) were randomized to receive either oral magnesium 15 mmol twice daily (Magnosolv-Granulat, total magnesium 365 mg provided as magnesium citrate) (n = 94) or placebo (n = 93) for 6 months. Symptom-limited exercise testing (Bruce protocol) and responses given on quality-of-life questionnaires were the outcomes measured. Magnesium therapy significantly increased intracellular magnesium levels ([Mg]i) in a substudy of 106 patients at 6 months compared with placebo (35.5 +/- 3.7 vs 32.6 +/- 2.9 mEq/L, p = 0.0151). Magnesium treatment significantly increased exercise duration time compared with placebo (8.7 +/- 2.1 vs 7.8 +/- 2.9 minutes, p = 0.0075), and lessened exercise-induced chest pain (8% vs 21%, p = 0.0237). Quality-of-life parameters significantly improved in the magnesium group. These findings suggest that oral magnesium supplementation in patients with CAD for 6 months results in a significant improvement in exercise tolerance, exercise-induced chest pain, and quality of life, suggesting a potential mechanism whereby magnesium could beneficially alter outcomes in patients with CAD.
Administration, Oral↗
Long-term outcome of intravenous magnesium therapy in thrombolysis-ineligible acute myocardial infarction patients.
The aim of our study was to analyze the long-term survival and cardiac function in 194 consecutive, thrombolysis-ineligible acute myocardial infarction (AMI) patients receiving 48-hour intravenous magnesium sulfate (22 g) - 96 patients, compared with placebo - 98 patients. After a mean 4.8-year follow-up, all-cause mortality and cardiac mortality were significantly lower in the magnesium compared to the placebo group [(18 vs. 33 patients, p < 0.01) and (12 vs. 30 patients, p < 0.001), respectively]. Rest radionuclide ventriculography tests for left-ventricular ejection fraction (LVEF) were assessed in surviving patients up to completion of follow-up. Magnesium-treated patients had a significantly higher LVEF (0.51 +/- 0.10 vs. 0.44 +/- 0.14, p < 0.05) and a lower incidence of heart failure compared to placebo-treated patients (12 vs. 3 patients, p = 0.02). Beneficial effects of intravenous magnesium therapy in thrombolysis-ineligible AMI patients appeared to last for at least 4.8 years, concomitant with preserved LVEF, suggesting a favorable role for acute magnesium treatment in these patients.
Aged↗
Does magnesium have a role in the treatment of patients with coronary artery disease?
Hypomagnesemia is common in hospitalized patients, especially in elderly patients with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with increased all cause mortality and mortality from CAD. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially confers upon magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. However, data regarding the use of magnesium in patients with acute myocardial infarction (AMI) are conflicting. Although some previous relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when intravenous magnesium was administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials (the Fourth International Study of Infarct Survival [ISIS 4] and Magnesium in Coronaries [MAGIC]) were unable to demonstrate any advantage of intravenous magnesium over placebo. Nevertheless, the theoretical benefits of magnesium supplementation as a cardio-protective agent in CAD patients, promising results from animal and human studies, its relatively low-cost and ease of handling requiring no special expertise, together with its excellent tolerability, gives magnesium a place in treating CAD patients, especially in those at high risk, such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as torsades de pointes and intractable ventricular tachycardia.
Aged↗
Endothelial dysfunction: a crystal ball prediction for enhanced cardiovascular risk?
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Cardiovascular Diseases↗
Noninvasive detection of collateral flow to the infarct-related coronary artery in patients after myocardial infarction by Tl-201 tomographic imaging.
BACKGROUND: The determination of viability and perfusion within the infarct zone in post-myocardial infarction patients has both therapeutic and prognostic significance. Reversibility of thallium 201 uptake within the territory of the infarct-related coronary artery (IRA) as shown by single photon emission computed tomography (SPECT) is associated with a jeopardized but viable myocardium. We aimed to test the hypothesis that for post-myocardial infarction patients undergoing Tl-201 stress-redistribution SPECT, a scintigraphic pattern of distal reversibility without proximal reversibility within a defect corresponding to the IRA territory is a marker of collateral flow to the occluded culprit artery. METHODS AND RESULTS: We assessed Tl-201 SPECT imaging results of 78 patients with IRA occlusion as demonstrated by angiography 7 +/- 1 months after myocardial infarction. Angiography demonstrated the presence of collateral flow in 57 patients and its absence in 21 patients. Distal reversibility was present in 42 of the 57 patients with collateral flow (sensitivity, 74%) and was absent in 16 of the 21 patients without collateral flow (specificity, 76%). Collateral flow to the IRA was demonstrated in 42 of 47 patients with distal reversibility (group A) (positive predictive value, 89%) and absent in 16 of 31 patients with a fixed defect without reversibility (group B) (P <.001) (negative predictive value, 52%). CONCLUSIONS: In patients after myocardial infarction, a Tl-201 SPECT redistribution pattern of distal reversibility without proximal reversibility within a defect in the IRA territory is a noninvasive marker of collateral flow to the culprit artery with a high positive predictive value that may provide valuable information on patient management. A larger prospective study in an unselected patient population is needed to further evaluate the clinical value of this marker.
Adult↗