The effect of smoking on myocardial performance index in middle-aged males after first acute myocardial infarction.

BACKGROUND: Cigarette smoking is associated with increased rates of coronary artery disease and acute myocardial infarction (MI). Paradoxically, smokers had lower mortality after MI. The purpose of this study was to evaluate the effect of chronic smoking on myocardial performance index (MPI) in middle-aged men after an acute MI. MATERIAL AND METHODS: A total of 429 patients (325 smokers vs. 104 nonsmokers) presenting with acute ST elevation MI were enrolled in this study. Thrombolysis in myocardial infarction (TIMI) flow of the infarct related artery was measured before and after the primary percutaneous coronary intervention (PCI), and Gensini score was also calculated. Conventional echocardiography and tissue Doppler echocardiography (TDI) were performed within 48-72 hours after onset of chest pain. Peak early (Em) and late (Am) diastolic velocities, peak systolic (Sm) mitral annular velocities and time intervals were recorded with TDI. The MPI, ratio of Em/Am, and E/Em were calculated. RESULTS: Baseline demographic and angiographic characteristics such as Gensini score, pre and, post PCI TIMI flow were similar in 2 groups. In contrast, LV MPI was preserved among smokers (0.59 ± 0.15 vs. 0.66 ± 0.14, P = 0.01), and Em/Am values were also higher in smokers (0.84 ± 0.28 vs. 0.75 ± 0.31, P = 0.01). Independent predictors of impaired MPI (≥0.60) were determined as nonsmoking status (odds ratio 2.940, 95% CI 0.98-5.83, P = 0.05), left anterior descending artery stenosis (odds ratio 3.196, 95% CI 1.73-5.91 P = 0.001), and, age (odds ratio 1.12, 95% CI 1.03-1.22, P = 0.01). CONCLUSIONS: Despite similar demographic and angiographic characteristics, smoker males had a paradoxically better MPI after acute MI.

Plasma concentrations of soluble CD40 ligand in smokers with acute myocardial infarction: a pilot study.

Coronary artery disease (CAD) is believed to be the single leading cause of death in both men and women in the world. Smoking is the most important risk factor for CAD. Smoking increases platelet aggregation and thrombus formation. CD40 ligand (CD40L) is a transmembrane glycoprotein derived from activated platelets. It participates in thrombus formation during the acute phase of acute myocardial infarction (MI). Elevation of CD40L identifies the patients who are at highest risk for cardiac events and who are likely to benefit from treatment with the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonists. The purpose of this study was to evaluate levels of CD40L in smokers with acute MI. Fifty-seven patients with acute MI were enrolled in this study. Thirty-one smokers were compared with 26 non-smokers. Soluble CD40L level in the plasma was determined by a standard enzyme-linked immunosorbent assay. Circulating levels of CD40L were higher in the smokers' group. Smokers with acute MI may have increased risk for thrombotic complications during acute MI, and optimal antiaggregant therapy should be administered.

Association between exaggerated blood pressure response to exercise and serum asymmetric dimethylarginine levels.

BACKGROUND: The exaggerated blood pressure response to exercise (EBPR) is an independent predictor of hypertension. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide inhibitor and higher plasma levels of ADMA are related to increased cardiovascular risk. The aim of this study is to identify the relationship between ADMA and EBPR. METHODS AND RESULTS: A total of 66 patients (36 with EBPR and 30 as controls) were enrolled in the study. EBPR is defined as blood pressure (BP) measurements > or =200/100 mmHg during the treadmill test. All the subjects underwent 24-h ambulatory BP monitoring. L-arginine and ADMA levels were measured using a high performance lipid chromatography technique. The serum ADMA levels were increased in the EBPR group compared to the healthy controls (4.0+/-1.4 vs 2.6+/-1.1 micromol/L respectively, P=0.001), but L-arginine levels were similar in the 2 groups (P=0.19). The serum ADMA levels were detected as an independent predictor of EBPR (odds ratio 2.28; 95% confidence interval 1.22-4.24; P=0.002). CONCLUSIONS: Serum ADMA levels might play a role in EBPR to exercise.

Exaggerated blood pressure response to exercise--a new portent of masked hypertension.

Masked hypertension (MHT) is a popular entity with increased risk of developing sustained hypertension, heart attack, stroke, and death. Subjects have normal blood pressure (BP) at office but elevated values at night so it is difficult to diagnose. Exaggerated blood pressure response to exercise (EBPR) is also a predictor of future hypertension. To investigate the relationship between these two entities, we evaluated 61 normotensive subjects with EBPR. The subjects underwent 24-h ambulatory blood pressure monitoring (ABPM). The prevalence of masked hypertension among subjects with EBPR was 41%. Body mass index (BMI), non-high density lipoprotein (HDL) cholesterol, diastolic blood pressure (DBP) at peak exercise and recovery, nondipping DBP pattern, and elevated early morning average BPs were associated with masked hypertension. In multivariate logistic regression analysis, the DBP measured at peak exercise was detected as an independent predictor of MHT in subjects with EBPR. Subjects with abnormally elevated BP during exercise are prone to MHT, necessitate medical assessment and close follow-up for hypertension.

The value of serum asymmetric dimethylarginine levels for the determination of masked hypertension in patients with diabetes mellitus.

BACKGROUND: An increased prevalence of masked hypertension (MHT) has been demonstrated among patients with diabetes mellitus (DM). MHT appears to cause cardiovascular (CV) complications similar to clinically overt hypertension. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide inhibitor and higher plasma levels of ADMA are related to increased CV risk in both the general population and among patients with DM. The aim of this study was to evaluate the relationship between MHT and ADMA in diabetic patients. METHODS: This study included DM patients (n = 131) with normal office blood pressure (<140/90 mmHg). None of the participants were using antihypertensive medications. All participants utilized an ambulatory blood pressure monitor (ABPM) for 24 h. Serum ADMA and arginine levels were measured using the fluorescence detector high performance liquid chromatography method. RESULTS: The prevalence of MHT was 24.4% among the study subjects. ADMA levels were increased in the MHT group when compared with normotensive diabetics (6.2 ± 2.2 vs 4.2 ± 1.7 µmol/L p = 0.001, respectively). Furthermore, arginine/ADMA ratio was lower in the MHT group than among the normotensive group (29.9 ± 12.1 vs 46.0 ± 19.0 p = 0.001). In the multivariate logistic regression model, ADMA, BMI and HDL levels were found to be independent predictors of MHT Odds ratio: 1.63 (1.28-2.06), 1.19 (1.05-1.35), and 0.95 (0.90-0.99), respectively. The cut-off value of the ADMA was 4.34 µmol/L with a sensitivity, specificity, positive predictive value, and negative predictive value of 84.4%, 59.6%, of 40.3%, and 92.2%, respectively (AUC = 0.78). CONCLUSIONS: Serum ADMA may play a role in both the pathophysiology and screening of MHT in DM subjects.

Assessment of the left atrial volume index and plasma NT-proANP level in patients with acute ST-elevation myocardial infarction.

OBJECTIVES: Acute ST-elevation myocardial infarction is associated with ventricular dysfunction due to ischemia-induced progressive myocardial damage. The decrease in ventricular compliance causes left atrial dilatation and stretching of the atrial myocardium, which are the main stimuli for the secretion of atrial natriuretic peptide. The aim of this study was to evaluate left atrial dimensions and atrial natriuretic peptide levels in patients early after their first acute ST-elevation myocardial infarction and assess the probable interaction between coronary lesions and these measurements. METHODS: A total of 110 patients with acute myocardial infarction and 50 controls were studied. Plasma atrial natriuretic peptide was measured at admission. Left ventricular function, diameter, and volume index were evaluated using transthoracic echocardiography. Gensini and vessel scores of the patients who underwent coronary angiography were calculated. RESULTS: Plasma atrial natriuretic peptide in the patients with myocardial infarction was increased compared with that in controls (3.90±3.75 vs. 1.35±0.72 nmol/L, p<0.001). Although the left atrial diameter was comparable in patients and controls, the left atrial volume index was increased in patients with acute myocardial infarction (26.5±7.1 vs. 21.3±4.9 mL/m2, p<0.01). Multivariate regression analysis showed a strong independent correlation between the left atrial volume index and the plasma atrial natriuretic peptide level (ß=0.23, p=0.03). CONCLUSIONS: The left atrial volume index and plasma atrial natriuretic peptide level were correlated in patients with acute myocardial infarction.

The effects of spironolactone on atrial remodeling in patients with preserved left ventricular function after an acute myocardial infarction: a randomized follow-up study.

OBJECTIVES: Atrial remodeling is an important part of cardiac remodeling after acute myocardial infarction (AMI). The aim of this study was to evaluate the effect of spironolactone on atria in patients with preserved left ventricular (LV) functions after AMI by using two-dimensional and tissue Doppler imaging techniques (TDI). METHODS: The study consisted of 110 patients with AMI, successfully revascularized with percutaneous coronary intervention, ejection fraction greater than or equal to 40%, and Killip class I-II. Patients were randomized into two groups: conventional therapy (n=55) and additional spironolactone of 25 mg/day with standard conventional therapy (n=55). Echocardiography was performed in the first 48-72 h of AMI and during 6 months of follow-up. Left atrial volume index and emptying fraction were obtained. The peak regional atrial contraction velocity, the time between the onset of p-wave on the monitor ECG and the onset, peak, and the end (TE) of the atrial contraction wave on the tissue Doppler technique curve were measured. RESULTS: The left atrial volume index and left atrium (LA) dimensions did not significantly change in either group. In the spironolactone group, left atrial emptying fraction increased compared with both baseline value (from 53.0 ± 0.16 to 57.0 ± 0.13 P=0.011) and conventional therapy group (from 50.0 ± 0.17 to 47.0 ± 0.16, P=0.013). The atrial contraction velocity did not change but the LA-TE, interatrial septum-TE, and right atrium-TE were prolonged in the conventional therapy group. CONCLUSION: Additional spironolactone therapy provided a little benefit on LA remodeling and atrial electromechanic properties in patients with AMI and preserved LV functions.

Complete atrioventricular block associated with rivastigmine therapy.

PURPOSE: A case of complete atrioventricular block associated with rivastigmine use is presented. SUMMARY: A 67-year-old Turkish woman with Alzheimer's disease was admitted to the hospital because of dizziness and syncope. Her medical history included diagnoses of hypertension (treated with amlodipine 5 mg daily) and diabetes mellitus (treated with nateglinide 120 mg daily). She had been taking both drugs for over five years. She had also been taking rivastigmine 6 mg p.o. daily for five months for the treatment of Alzheimer's disease. She had experienced dizziness since the onset of rivastigmine therapy but had not reported it to any health care provider. On admission, she had a blood pressure measurement of 90/60 mm Hg and a pulse rate of 34 beats/min. A 12-lead electrocardiogram revealed complete atrioventricular block. Echocardiography results, blood electrolyte levels, and cardiac biochemical markers were normal. After initial evaluation, a temporary transvenous pacemaker was implanted via the right femoral vein. Amlodipine and rivastigmine were discontinued. On the first day of hospitalization, a coronary angiogram revealed normal coronary anatomy. Two days later, the complete atrioventricular block resolved spontaneously to sinus rhythm. Rivastigmine 6 mg p.o. daily was reinitiated, and complete atrioventricular block recurred on the fourth day of therapy. A VVI permanent pacemaker was implanted on the fifth day of hospitalization. Amlodipine and rivastigmine were reinitiated. The patient continued rivastigmine 6 mg p.o. daily after permanent pacemaker implantation. A three-month follow-up appointment revealed that no further syncope episodes or dizziness had occurred. CONCLUSION: A 67-year-old woman developed complete atrioventricular block after receiving rivastigmine for the treatment of Alzheimer's disease.

Assessment of the left atrial volume index and plasma NT-proANP level in patients with acute ST-elevation myocardial infarction

OBJECTIVES: Acute ST-elevation myocardial infarction is associated with ventricular dysfunction due to ischemia-induced progressive myocardial damage. The decrease in ventricular compliance causes left atrial dilatation and stretching of the atrial myocardium, which are the main stimuli for the secretion of atrial natriuretic peptide. The aim of this study was to evaluate left atrial dimensions and atrial natriuretic peptide levels in patients early after their first acute ST-elevation myocardial infarction and assess the probable interaction between coronary lesions and these measurements. METHODS: A total of 110 patients with acute myocardial infarction and 50 controls were studied. Plasma atrial natriuretic peptide was measured at admission. Left ventricular function, diameter, and volume index were evaluated using transthoracic echocardiography. Gensini and vessel scores of the patients who underwent coronary angiography were calculated. RESULTS: Plasma atrial natriuretic peptide in the patients with myocardial infarction was increased compared with that in controls (3.90±3.75 vs. 1.35±0.72 nmol/L, p<0.001). Although the left atrial diameter was comparable in patients and controls, the left atrial volume index was increased in patients with acute myocardial infarction (26.5±7.1 vs. 21.3±4.9 mL/m2, p<0.01). Multivariate regression analysis showed a strong independent correlation between the left atrial volume index and the plasma atrial natriuretic peptide level (β = 0.23, p = 0.03). CONCLUSIONS: The left atrial volume index and plasma atrial natriuretic peptide level were correlated in patients with acute myocardial infarction. .