The novel finding is that OSA may inhibit the recovery of LV function in patients with AMI.

Objective The object of our study was to identify the most useful predictor of patient prognosis in acute myocardial infarction (AMI), from 7 acute-phase cardiovascular peptides which take part in neurohumoral activation [brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), renin, aldosterone, adrenomedullin, epinephrine and norepinephrine].Methods In 141 consecutive AMI patients, 24 hours from onset, we evaluated plasma concentration levels of the 7 types of cardiovascular peptides and the relationships between the values of these peptides and short-term clinical prognosis, including mortality.Results Plasma levels of all cardiovascular peptides were significantly higher in patients who suffered mortality than in surviving patients (BNP: 1,267±997 pg/ml vs. 293±327 pg/ml, p<0.0001; ANP: 164±186 pg/ml vs. 64±76 pg/ml, p<0.001; adrenomedullin: 13.61±3.29 Fmol/l vs. 3.45±1.52 Fmol/l, p<0.0001; renin: 8.79±7.15 ng/ml/h vs. 4.34±5.10 ng/ml/h, p<0.01; aldosterone: 249±210 pg/ml vs. 68±74 pg/ml, p<0.0001; epinephrine: 3,191±8,360 pg/ml vs. 68±74 pg/ml, p<0.0001; norepinephrine: 21.

SUMMARYDespite increased risk for coronary artery disease and acute myocardial infarction (AMI), prior studies have found that smokers with AMI have lower mortality rates than nonsmokers, a phenomenon often termed 'smoker's paradox'. The present study was designed to examine the etiology of 'smoker's paradox', especially with respect to the association with inflammation.The subjects included 528 consecutive AMI patients who were admitted within 24 hours of onset and underwent successful coronary intervention. Of the 528 subjects, 232 (44%) were smokers.The cardiac mortality rates over a 6 month period was significantly lower in the smoking group than the nonsmoking group (3% versus 9%, P = 0.01). There were significantly more male patients in the smoking group, and the smoking group was significantly younger than the nonsmoking group (P < 0.0001). The value of high sensitivity C-reactive protein (hs-CRP) on admission and 24 hours after onset, and serum amyloid A protein (SAA) were significantly higher, and acute phase BNP was significantly lower (hs-CRP on admission 1.36 ± 1.03 mg/dL versus 0.75 ± 0.82 mg/dL, P = 0.02, hs-CRP at 24 hours 3.86 ± 4.32 mg/dL versus 2.90 ± 3.46 mg/dL, P = 0.008, SAA; 288 ± 392 µg/dL versus 176 ± 206 µg/dL, P < 0.05, BNP; 248 ± 342 pg/mL versus 444 ± 496 pg/mL, P = 0.0002) in the smoking group than in the nonsmoking group. The early ST-segment resolution rate was higher in the smoking group compared with the nonsmoking group (80% versus 66%, P = 0.003).The reason why smokers with AMI have lower mortality rates than nonsmokers, the so-called 'smoker's paradox', is believed to be because smoking induces inflammation and smokers may have less damage to microvascular function after primary percutaneous coronary intervention. (Int Heart J 2008; 49: 13-24) Key words: Myocardial infarction, Smoking, Inflammation EVEN though many epidemiologic studies have shown that cigarette smoking is associated with higher rates of myocardial infarction and death from coronary From the

ndothelins (ET) are 21-amino-acid peptides produced by the endothelium and which play important roles in cardiovascular physiology and pathophysiology. 1 The most important ET produced by the endothelium is ET-1, which has an important role in the vasoconstriction of the peripheral arterial system and also of the coronary vascular bed. 2 Elevated plasma concentrations of ET have been observed in patients suffering from diverse cardiovascular diseases, such as congestive heart failure, 3-5 pulmonary hypertension 6 and angina pectoris. [7][8][9] In patients with acute myocardial infarction (AMI) particularly, the cardiac ET system is markedly activated 10,11 and plasma concentrations of ET-1 are elevated. 12 Little is known, however, about the relationship between plasma ET-1 concentrations, mortality and left ventricular (LV) systolic function in human AMI subjects.The object of the present study was to determine whether clinical prognosis after AMI may be predicted from acutephase plasma ET-1 concentrations, and to assess whether there might be any relationship between plasma ET-1 concentrations and LV systolic function. Methods Patient PopulationThe study population comprised 110 consecutive patients (79 males, 31 females; 68±11 years, range 40-93) presenting with a first AMI, admitted and enrolled between March 2003 and June 2004. Diagnosis of AMI was done according to the following criteria: (1) complaint of chest pain and/or discomfort; (2) electrocardiographic ST segment elevation of ≥0.1 mV in 2 or more limb leads, or ≥0.2 mV in 2 or more precordial leads, or new left bundlebranch block; and (3) elevation of total serum creatine kinase (CK) more than twice the upper limit of the normal range. We excluded patients with renal failure on admission (serum creatinine >2.5 mg/dl), patients with old myocardial infarction (MI), patients who reached the institution >6 h after onset, and patients who died <24 h after onset (ie, at the time of blood sampling). We diagnosed anterior MI in 54 patients. Subjects were divided into 2 groups according to the median plasma ET-1 concentration: <2.9 pg/ml (L group, n=55) and ≥2.9 pg/ml (H group, n=55). We distinguished between angina pectoris episodes <24 h before the onset of AMI from general angina pectoris, to take into account ischemic pre-conditioning. Treatment StrategyFollowing oral administration of 200 mg of aspirin and 200 mg of ticlopidine, all patients successfully underwent direct percutaneous coronary intervention (PCI) within 8 h of the onset of symptoms. In 18 patients, conventional plain

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