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1.  Cardiogenic SHOCK Without Flow-Limiting Angiographic Coronary Artery Disease – (From The SHOCK Trial And Registry) 
Myocardial infarction (MI) often develops when thrombosis occurs at lesions which have not previously been flow-limiting. However, the development of cardiogenic shock complicating acute myocardial infarction in such circumstances has received little attention. We studied the characteristics of 15 patients with cardiogenic shock who had no flow-limiting angiographic stenosis compared to 767 patients with at least one stenosis, who were enrolled in the SHOCK Trial and Registry. Compared to patients with at least one flow-limiting stenosis, patients with no flow-limiting stenosis were less likely to have pulmonary edema on chest x-ray (29% v 62%, P=0.008), and to have white ethnicity (53% v 82%, P = 0.011), and had lower median highest creatine kinase levels (702 v 2731 u/l; P = 0.018). For SHOCK Trial patients 1-year survival was 49% for patients with at least one flow-limiting stenosis and 71% for those with no flow-limiting stenosis (P= 0.268).
doi:10.1016/j.amjcard.2009.03.002
PMCID: PMC4060258  PMID: 19576316
no flow-limiting stenosis; myocardial infarction; cardiogenic shock
2.  New ST-depression: an under-recognized high-risk category of ‘complete’ ST-resolution after reperfusion therapy 
Aim:
It is not known if there is an association between resolution of ST-elevation to ST-depression following fibrinolysis and 30-day mortality.
Methods:
In an ECG substudy of HERO-2, which compared bivalirudin to unfractionated heparin following streptokinase in 12,556 patients with ST-elevation myocardial infarction ECGs were recorded at baseline and at 60 minutes after commencing fibrinolysis. The main outcome measure was 30-day mortality.
Results:
Using summed ST-segment elevation and five categories of changes in the infarct leads, further ST-elevation, 0–30% ST-resolution, >30–70% (partial) ST-resolution, >70% (complete) ST-resolution, and new ST-depression occurred in 21.7, 24.9, 36.8, 14.8, and 1.8% of patients, with 30-day mortality of 12.3, 11.7, 8.0, 4.2, and 8.1%, respectively. For the comparison of new ST-depression with complete ST-resolution and no ST-depression, p<0.01 with 24-hour mortality 4.5 vs. 1.3%, respectively (p=0.0003). Patients with new ST-depression had similar peak cardiac enzyme elevations as patients with complete ST-resolution without ST-depression. On multivariate analysis including summed ST-elevation at baseline, age, sex, and infarct location, new ST-depression was a significant predictor of 30-day mortality (OR 1.82, 95% CI 1.42–4.29).
Conclusions:
In patients with complete ST-resolution following fibrinolysis, new ST-depression at 60 minutes developed in 10.8% of patients. These patients had higher mortality than patients with complete ST-resolution without ST-depression and represent a high-risk group which could benefit from rapid triage to early angiography and revascularization as appropriate.
doi:10.1177/2048872612454841
PMCID: PMC3760535  PMID: 24062909
Fibrinolysis; mortality; new ST-depression
3.  Rapid Complete Reversal of Systemic Hypoperfusion following Intra-Aortic Balloon Pump Counterpulsation and Survival in Cardiogenic Shock Complicating an Acute Myocardial Infarction 
American heart journal  2011;162(2):268-275.
Background
In patients with cardiogenic shock (CS) complicating an acute myocardial infarction, a strategy of emergency revascularization vs. initial medical stabilization improves survival. Intra-aortic balloon counterpulsation (IABC) provides hemodynamic support and facilitates coronary angiography and revascularization in CS patients.
Methods and Results
We evaluated 499 patients with record of systemic hypoperfusion status, as an early response to IABC from the SHOCK Trial (n=185) and Registry (n=314) to determine the association between rapid complete reversal of systemic hypoperfusion following 30 minutes of IABC(CRH)and 30-day and 1-year mortality. CRH was highly associated with lower 30-day mortality (45% vs. 78%, p<0.001) in all patients. In the SHOCK Trial, among patients assigned to ERV vs. IMS, 30-day mortality was 26% vs. 29% with CRH, and 61% vs. 81% respectively without CRH, after commencing IABC. The corresponding 1-year mortality rates were 35% vs. 52% for ERV and 69% vs. 87% for IMS (interaction p ≥ 0.25 at both time points). After adjusting for important correlates of outcome (LV ejection fraction, age, and randomization to ERV) a significant association remained between CRH and 30-day mortality (odds ratio 0.18; 95% CI 0.08–0.42, p<0.001) and 1-year mortality (odds ratio 0.28; 95% CI 0.12–0.67, p<0.001).
Conclusions
In CS patients, CRH after commencing IABC was independently associated with improved 30-day and 1-year survival regardless of emergency revascularization. In CS patients, CRH with IABC is an important early prognostic feature.
doi:10.1016/j.ahj.2011.04.025
PMCID: PMC3155687  PMID: 21835287
cardiogenic shock; intra-aortic balloon counterpulsation; systemic hypoperfusion; survival
4.  aVR ST elevation: an important but neglected sign in ST elevation acute myocardial infarction 
European Heart Journal  2010;31(15):1845-1853.
Aim
This study evaluated the prognostic implications of aVR ST elevation during ST elevation acute myocardial infarction (AMI).
Methods and results
The Hirulog and Early Reperfusion/Occlusion-2 study randomized 17 073 patients with acute ST elevation AMI within 6 h of symptom onset to receive either bivalirudin or heparin, in addition to streptokinase and aspirin. The treatments had no effect on the primary endpoint of 30-day mortality. Electrocardiographic recordings were performed at randomization and at 60 min after commencing streptokinase. aVR ST elevation ≥1 mm was associated with higher 30-day mortality in 15 315 patients with normal intraventricular conduction regardless of AMI location (14.7% vs. 11.2% for anterior AMI, P = 0.0045 and 16.0% vs. 6.4% for inferior AMI, P < 0.0001). After adjusting for summed ST elevation and ST depression in other leads, associations with higher mortality were found with aVR ST elevation of ≥1.5 mm for anterior [odds ratio 1.69 (95% CI 1.16 to 2.45)] and of ≥1 mm for inferior AMI [odds ratio 2.41 (95% CI 1.76 to 3.30)]. There was a significant interaction between aVR ST elevation and infarct location. Thirty-day mortality was similar with anterior and inferior AMI when aVR ST elevation was present (11.5% vs. 13.2%, respectively, P = 0.51 with 1 mm and 23.5% vs. 22.5% respectively, P = 0.84 with ≥ 1.5 mm ST elevation). After fibrinolytic therapy, resolution of ST elevation in aVR to <1 mm was associated with lower mortality, while new ST elevation ≥1 mm was associated with higher mortality.
Conclusion
aVR ST elevation is an important adverse prognostic sign in AMI.
doi:10.1093/eurheartj/ehq161
PMCID: PMC2913115  PMID: 20513728
Electrocardiography; Mortality; Myocardial infarction
5.  The compression type of coronary artery motion in patients with ST-segment elevation acute myocardial infarction and normal controls: a case-control study 
BMC Research Notes  2011;4:51.
Background
Prediction of the location of culprit lesions responsible for ST-segment elevation myocardial infarctions may allow for prevention of these events. A retrospective analysis of coronary artery motion (CAM) was performed on coronary angiograms of 20 patients who subsequently had ST-segment elevation myocardial infarction treated by primary or rescue angioplasty and an equal number of age and sex matched controls with normal angiograms.
Findings
There was no statistically significant difference between the frequency of CAM types of the ST-segment elevation acute myocardial infarction and control patients (p = 0.97). The compression type of CAM is more frequent in the proximal and mid segments of all three coronary arteries. No statistically significant difference was found when the frequency of the compression type of CAM was compared between the ST-segment elevation acute myocardial infarction and control patients for the individual coronary artery segments (p = 0.59).
Conclusion
The proportion of the compression type of coronary artery motion for individual artery segments is not different between patients who have subsequent ST-segment elevation myocardial infarctions and normal controls.
doi:10.1186/1756-0500-4-51
PMCID: PMC3063224  PMID: 21385385
6.  Bilateral coronary - pulmonary fistulae, diagnosed by transoesophageal echocardiogram 
Heart International  2010;5(2):e14.
Bilateral coronary artery fistulae to pulmonary artery is a rare condition. We diagnosed this condition by transoesophageal echocardiogram and successfully treated with surgery.
doi:10.4081/hi.2010.e14
PMCID: PMC3184687  PMID: 21977299
Fistula; coronary artery; pulmonary artery; echocardiography.
7.  Biophysical Properties of 9 KCNQ1 Mutations Associated with Long QT Syndrome (LQTS) 
Background
Inherited long QT syndrome (LQTS) is characterized by prolonged QT interval on the EKG, syncope and sudden death due to ventricular arrhythmia. Causative mutations occur mostly in cardiac potassium and sodium channel subunit genes. Confidence in mutation pathogenicity is usually reached through family genotype-phenotype tracking, control population studies, molecular modelling and phylogenetic alignments, however, biophysical testing offers a higher degree of validating evidence.
Methods and Results
By using in-vitro electrophysiological testing of transfected mutant and wild-type LQTS constructs into Chinese Hamster Ovary cells, we investigated the biophysical properties of 9 KCNQ1 missense mutations (A46T, T265I, F269S, A302V, G316E, F339S, R360G, H455Y, and S546L) identified in a New Zealand based LQTS screening programme. We demonstrate through electrophysiology and molecular modeling that seven of the missense mutations have profound pathological dominant negative loss-of-function properties confirming their likely disease-causing nature. This supports the use of these mutations in diagnostic family screening. Two mutations (A46T, T265I) show suggestive evidence of pathogenicity within the experimental limits of biophysical testing, indicating that these variants are disease-causing via delayed or fast activation kinetics. Further investigation of the A46T family has revealed an inconsistent co-segregation of the variant with the clinical phenotype.
Conclusions
Electrophysiological characterisation should be used to validate LQTS pathogenicity of novel missense channelopathies. When such results are inconclusive, great care should be taken with genetic counselling and screening of such families, and alternative disease causing mechanisms should be considered.
doi:10.1161/CIRCEP.109.850149
PMCID: PMC2748886  PMID: 19808498
Long QT; Mutations; Arrhythmia; Ion Channels; Sudden Cardiac Death

Results 1-10 (10)