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Burchill L.J.,University of Melbourne | Burchill L.J.,Peter Munk Cardiac Center | Velkoska E.,University of Melbourne | Dean R.G.,University of Melbourne | And 3 more authors.
Clinical Science | Year: 2012

The RAS (renin-angiotensin system) is activated after MI (myocardial infarction), and RAS blockade with ACEis [ACE (angiotensin-converting enzyme) inhibitors] or ARBs (angiotensin receptor blockers) slows but does not completely prevent progression to heart failure. Cardiac ACE is increased after MI and leads to the formation of the vasoconstrictor AngII (angiotensin II). The enzyme ACE2 is also activated after MI and degrades AngII to generate the vasodilator Ang-(1-7) [angiotensin-(1-7)]. Overexpression of ACE2 offers cardioprotective effects in experimental MI, but there is conflicting evidence as to whether the benefits of ACEis and ARBs are mediated through increasing ACE2 after MI. In the present study, we assessed the effect of an ACEi and ARB, alone and in combination, on cardiac ACE2 in a rat MI model. MI rats received vehicle, ACEi (ramipril; 1 mg/kg of body weight), ARB (valsartan; 10 mg/kg of body weight) or combination (ramipril at 1 mg/kg of body weight and valsartan at 10 mg/kg of body weight) orally for 28 days. Sham-operated rats were also studied and received vehicle alone. MI increased LV (left ventricular) mass (P < 0.0001), impaired cardiac contractility (P < 0.05) and activated cardiac ACE2 with increased gene (P < 0.05) and protein expression (viable myocardium, P < 0.05; border zone, P < 0.001; infarct, P < 0.05). Ramipril and valsartan improved remodelling (P < 0.05), with no additional effect of dual therapy. Although ramipril inhibited ACE, and valsartan blocked the angiotensin receptor, neither treatment alone nor in combination augmented cardiac ACE2 expression. These results suggest that the cardioprotective effects of ramipril and valsartan are not mediated through up-regulation of cardiac ACE2. Strategies that do augment ACE2 after MI may be a useful addition to standard RAS blockade after MI. © The Authors Journal compilation © 2012 Biochemical Society. Source

Mather A.N.,University of Leeds | Crean A.,Peter Munk Cardiac Center | Abidin N.,University of Salford | Worthy G.,University of Leeds | And 3 more authors.
Journal of Cardiovascular Magnetic Resonance | Year: 2010

Background: Improved outcomes for normoglycemic patients suffering acute myocardial infarction (AMI) over the last decade have not been matched by similar improvements in mortality for diabetic patients despite similar levels of baseline risk and appropriate medical therapy. Two of the major determinants of poor outcome following AMI are infarct size and left ventricular (LV) dysfunction. Methods. Ninety-three patients with first AMI were studied. 22 patients had diabetes mellitus (DM) based on prior history or admission blood glucose 11.1 mmol/l. 13 patients had dysglycemia (admission blood glucose 7.8 mmol/l but <11.1 mmol/l) and 58 patients had normoglycemia (admission blood glucose <7.8 mmol/l). Patients underwent cardiac magnetic resonance (CMR) imaging at index presentation and median follow-up of 11 months. Cine imaging assessed LV function and late gadolinium contrast-enhanced imaging was used to quantify infarct size. Clinical outcome data were collected at 18 months median follow-up. Results: Patients with dysglycemia and DM had larger infarct sizes by CMR than normoglycemic patients; at baseline percentage LV scar (mean (SD)) was 23.0% (10.9), 25.6% (12.9) and 15.8% (10.3) respectively (p = 0.001), and at 11 months percentage LV scar was 17.6% (8.9), 19.1% (9.6) and 12.4% (7.8) (p = 0.017). Patients with dysglycemia and DM also had lower event-free survival at 18 months (p = 0.005). Conclusions: Patients with dysglycemia or diabetes mellitus sustain larger infarct sizes than normoglycemic patients, as determined by CMR. This may, in part, account for their adverse prognosis following AMI. © 2010 Mather et al; licensee BioMed Central Ltd. Source

Grube E.,University of Bonn | Chevalier B.,Institute Hospitalier Jacques Cartier | Smits P.,Maasstad Ziekenhuis | Davk V.,Peter Munk Cardiac Center | And 6 more authors.
JACC: Cardiovascular Interventions | Year: 2011

Objectives: The SPIRIT V (A Clinical Evaluation of the XIENCE V Everolimus-Eluting Coronary Stent System in the Treatment of Patients With De Novo Coronary Artery Lesions) study is a post-market surveillance experience of the XIENCE V (Abbott Vascular, Santa Clara, California) everolimus-eluting stent (EES) in patients with higher-risk coronary anatomy. Background: Previous pre-approval studies have shown the safety and efficacy of EES in highly selected groups of patients. Methods: The SPIRIT V trial is a prospective, open label, single arm, multicenter study. Two thousand seven hundred patients with multiple de novo coronary artery lesions suitable for treatment with a planned maximum of 4 EES were enrolled at 93 centers in Europe, Asia Pacific, Canada, and South Africa. Lesions had a reference vessel diameter between 2.25 and 4.0 mm and a length of ≤28 mm by visual estimation. An independent clinical events committee adjudicated all end point-related events. The primary end point was the composite rate of all death, myocardial infarction (MI), and target vessel revascularization at 30 days. Secondary end points included stent thrombosis and acute success (clinical device and procedure success). Results: At 30 days, the primary composite end point of all death, MI, and target vessel revascularization was 2.7%. At 1 year, rates of cardiac death, overall MI, and target lesion revascularization were 1.1%, 3.5%, and 1.8%, respectively. The cumulative rate of definite and probable stent thrombosis was low at 0.66% at 1 year. Conclusions: Use of EES in patients with multiple, complex de novo lesions yielded 1-year major adverse cardiac events, stent thrombosis, and target lesion revascularization rates that are comparable to those of the more controlled SPIRIT II and SPIRIT III trialswhich included patients with restricted inclusion/exclusion criteriaand other all-comer population, physician-initiated studies like the X-SEARCH (Xience Stent Evaluated At Rotterdam Cardiology Hospital) and COMPARE (A Randomized Controlled Trial of Everolimus-eluting Stents and Paclitaxel-eluting Stents for Coronary Revascularization in Daily Practice) trials. © 2011 American College of Cardiology Foundation. Source

Urbano-Moral J.A.,Tufts Medical Center | Rowin E.J.,Tufts Medical Center | Maron M.S.,Tufts Medical Center | Crean A.,Peter Munk Cardiac Center | Pandian N.G.,Tufts Medical Center
Circulation: Cardiovascular Imaging | Year: 2014

Background-In hypertrophic cardiomyopathy (HCM), heterogeneous myocardial hypertrophy and fibrosis are responsible for abnormalities of left ventricular (LV) function. We aimed to characterize LV global and regional myocardial mechanics in HCM, according to segmental hypertrophy and fibrosis. Methods and Results-Fifty-nine patients with HCM underwent standard echocardiography, 3-dimensional speckle tracking echocardiography, and cardiac magnetic resonance with late gadolinium enhancement (LGE); all 3 tests were <24 hours apart. Longitudinal, circumferential, and area strains were investigated according to the extent of LGE (no LGE, LGE<10%, and LGE≥10%), segmental thickness (≥15 versus <15 mm), and segmental LGE (LGE versus non-LGE). Attenuated global longitudinal strain showed association with extent of hypertrophy (indexed LV mass, r=0.32, P=0.01; maximum LV wall thickness, r=0.34, P=0.009; number of segments ≥15 mm, r=0.44, P<0.001), whereas enhanced global circumferential strain was correlated to LV global functional parameters (indexed end-systolic volume, r=0.47, P<0.001; ejection fraction, r=-0.75, P<0.001). Parameters of global myocardial mechanics showed no association with the extent of LGE; in contrast, the extent of LGE was associated with the extent of hypertrophy. All 3 deformation parameters were attenuated both in segments =15 mm in thickness and in those with LGE; adjusted analysis demonstrated that segmental presence of LGE was associated with additional attenuation in myocardial deformation. Conclusions-Both hypertrophy and fibrosis contribute to regional impairment of myocardial shortening in HCM. The extent of hypertrophy is the primary factor altering global myocardial mechanics. Circumferential myocardial shortening seems to be directly involved in preservation of LV systolic performance in HCM. © 2013 American Heart Association, Inc. Source

Ayling O.,Peter Munk Cardiac Center | Martin A.,Toronto Western Hospital | Roche-Nagle G.,Peter Munk Cardiac Center | Roche-Nagle G.,University of Toronto
Vascular and Endovascular Surgery | Year: 2014

Traumatic superficial temporal artery (STA) pseudoaneurysm is a rare clinical entity that typically presents after a short delay following blunt trauma. Diagnosis should be made primarily upon history and physical examination while duplex ultrasound is an appropriate adjunct for confirmation and preoperative planning. Optimal management of traumatic STA pseudoaneurysm is surgical and may consist of ligation and excision of the aneurysmal artery or, alternatively, primary arterial repair when feasible. Surgical treatment is usually possible under local anesthetic alone and is usually curative while incurring minimal risk of complications. © The Author(s) 2014. Source

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