Natalie Cutri

ST/T wave changes during acute coronary syndrome presentation in patients with the coronary slow flow phenomenon

Article history:Received 20 October 2010Accepted 23 October 2010Available online 3 December 2010Keywords:Coronary slow flow phenomenonECG abnormalitiesAcute coronary syndromeMyocardial ischaemia⁎ Corresponding author. Cardiology Unit, The Queen Elizabeth Hospital, 28 Wood-ville Road, Woodville, SA 5011, Australia. Tel.: +61 8222 6740; fax: +61 8222 6042.E-mail address: john.beltrame@adelaide.edu.au (J.F. Beltrame).Table 1Baseline characteristics.CSFP ControlsNumber 37 20Age (Mean±SD) 49±14.6*years 54.8±13.5 yearsCV risk factorsMales 27 (73%)* 9 (45%)Smoking History 19 (51%) 5 (25%)Hypertension 19 (51%)** 0 (0%)Cholesterol 20 (54%)* 6 (30%)Diabetes 9 (24%) 1 (5%)Pain-free Resting ECGSinus Rhythm 33 (100%) 20 (100%)Heart Rate 65±10 bpm 60±7 bpmResting ST changes 13 (39%)** 0 (0%)Inferior ST Elevation 9 (27%)* 0 (0%)Anterior ST Elevation 1 (3%) 0 (0%)Resting T wave changes 5 (15%) 1 (5%)Inferior T wave change 2 (6%) 1 (3%)Anterior T wave change 2 (6%) 0 (0%)QTc Interval 426±33 msec 410±10 msec*pb0.05 or **pb0.01; significant difference between CSFPs and healthy controls.

The role of nitric oxide in the coronary slow flow phenomenon.

The coronary slow flow phenomenon (CSFP) is a coronary microvascular disorder angiographically defined by the delayed passage of contrast within the epicardial arteries, despite the absence of obstructive coronary artery disease. Although several approaches have been used to operationally define this disorder [1], all embrace the concept of impaired angiographic contrast flow due to increased coronary microvascular resistance. This microvascular dysfunction differs from many other coronary microvascular disorders since coronary haemodynamic studies have demonstrated (a) increased resting microvascular resistance [2,3], (b) preserved vasodilator capacity (i.e. coronary flow reserve) [2,3] and (c) dynamic microvascular dysfunction, as vasodilator therapy acutely improves the angiographic phenomenon [4]. Furthermore, as the CSFP not only differs haemodynamically but also clinically from other primary coronary microvascular disorders [4], it warrants consideration as a novel form of primary microvascular angina [4,5].

Quality of Life Outcomes in Chronic Stable Angina Patients Treated with PCI or Medical Therapy

was associated with higher mortality. Unadjusted, each 0.5mm step increase in V1 ST level was associated with ∼25% increase in 30-day mortality and this was true for patients with and patients without V3 ST depression. The odds ratio for mortality was 1.21 (95% confidence interval 1.07–1.37) after adjusting for infero-lateral ST elevation and clinical factors and 1.24 (95% confidence interval 1.09–1.40) if also adjusted to V3 ST level. In contrast lead V1 ST depression was not associated with mortality after adjustment for V3 ST level. V1 ST elevation ≥1mm, analyzed dichotomously in all patients, was significantly associated with higher mortality (28% higher unadjusted, 51% higher adjusted to V3 ST level, and 35% higher adjusted to ECG and clinical factors). Resolution of V1 ST elevation ≥1mm 60min after fibrinolysis was associated with lower mortality (5.5% vs 10.8%, P= 0.0012). Conclusion: V1 ST elevation identifies higher risk patients with inferior AMI. doi:10.1016/j.hlc.2009.05.276