Microvascular resistance predicts myocardial salvage and infarct characteristics in ST-elevation myocardial infarction

<b>Background:</b> The pathophysiology of myocardial injury and repair in patients with ST‐elevation myocardial infarction is incompletely understood. We investigated the relationships among culprit artery microvascular resistance, myocardial salvage, and ventricular function.<p></p> <b>Methods and Results:</b> The index of microvascular resistance (IMR) was measured by means of a pressure‐ and temperature‐sensitive coronary guidewire in 108 patients with ST‐elevation myocardial infarction (83% male) at the end of primary percutaneous coronary intervention. Paired cardiac MRI (cardiac magnetic resonance) scans were performed early (2 days; n=108) and late (3 months; n=96) after myocardial infarction. T2‐weighted‐ and late gadolinium–enhanced cardiac magnetic resonance delineated the ischemic area at risk and infarct size, respectively. Myocardial salvage was calculated by subtracting infarct size from area at risk. Univariable and multivariable models were constructed to determine the impact of IMR on cardiac magnetic resonance–derived surrogate outcomes. The median (interquartile range) IMR was 28 (17–42) mm Hg/s. The median (interquartile range) area at risk was 32% (24%–41%) of left ventricular mass, and the myocardial salvage index was 21% (11%–43%). IMR was a significant multivariable predictor of early myocardial salvage, with a multiplicative effect of 0.87 (95% confidence interval 0.82 to 0.92) per 20% increase in IMR; P<0.001. In patients with anterior myocardial infarction, IMR was a multivariable predictor of early and late myocardial salvage, with multiplicative effects of 0.82 (95% confidence interval 0.75 to 0.90; P<0.001) and 0.92 (95% confidence interval 0.88 to 0.96; P<0.001), respectively. IMR also predicted the presence and extent of microvascular obstruction and myocardial hemorrhage.<p></p> <b>Conclusion:</b> Microvascular resistance measured during primary percutaneous coronary intervention significantly predicts myocardial salvage, infarct characteristics, and left ventricular ejection fraction in patients with ST‐elevation myocardial infarction.<p></p&gt

Pathophysiology of myocardial remodeling in survivors of ST-elevation myocardial infarction revealed by native T1 mapping: inflammation, remote myocardium and prognostic significance

Background: The pathophysiology and prognostic significance of remote myocardium in the natural history of STEMI is uncertain. Cardiac magnetic resonance (CMR) provides a non-invasive assessment of myocardial pathology that is spatially and temporally coordinated. Native T1 quantified by CMR (T1 relaxation time, milliseconds) is a fundamental tissue property determined by water content and cellularity. We aimed to investigate the clinical significance of remote myocardium in survivors of acute ST-elevation myocardial infarction (STEMI) using native T1 mapping. Methods: We performed a prospective single center cohort study in reperfused STEMI patients who underwent CMR 2 days and 6 months post-MI and long term follow-up (18 months minimum). Native T1 CMR (MOLLI investigational prototype sequence: 3 (3) 3 (3) 5) was measured in regions-of-interest in remote and injured myocardium. Infarction was depicted on late gadolinium contrast enhancement imaging. Adverse remodeling was defined as an increase in left ventricular end-diastolic volume ≥ 20% at 6 months. Major adverse cardiac events (MACE) were defined as cardiac death or hospitalization for non-fatal MI or heart failure. Results are mean±SD unless specified. Results: 300 STEMI patients (mean age 59 years, 74% male) gave informed consent (14 July 2011 - 21 November 2012). Of these, 288 STEMI patients had evaluable native T1 CMR and follow-up data (median duration 845 days). Infarct size was 18±14% of left ventricular mass. Two days post-STEMI, native T1 in remote myocardium was lower than native T1 in the infarct zone (961±25 ms vs. 1097±52 ms; p<0.01). In multivariable linear regression, remote zone native T1 was independently associated with incomplete ST-segment resolution (9.42 (2.37 to 16.47); p=0.009), the log of the initial CRP concentration (regression coefficient 3.01 (95% CI 0.016 to 5.55); p=0.038) and the peak monocyte count within 2 days of admission (10.20 (0.74, 19.67); p=0.035). At 6 months, left ventricular end-diastolic volume increased by 5 (25) ml (n=262 patients with evaluable data) overall, and adverse remodeling occurred in 30 (12%) patients. Remote zone native T1 was a multivariable predictor of the change in left ventricular end-diastolic volume from baseline (0.13 (0.01, 0.24); p=0.035). 39 (13.5%) patients experienced a MACE including 20 (6.9%) patients with a post-discharge MACE. Remote zone native T1 was an independent predictor of post-discharge MACE (hazard ratio 1.016, 95% CI 1.000, 1.032; p=0.048) including after adjustment for changes in LVEF (p=0.032), LV end-diastolic volume (p=0.053), and monocyte count (p=0.036). Conclusions: Remote zone tissue characteristics early post-MI are temporally linked with reperfusion injury and inflammation and independently predict left ventricular remodeling and MACE in STEMI survivors

Late gadolinium enhancement and adverse outcomes in a contemporary cohort of adult survivors of tetralogy of Fallot

Objective: Myocardial fibrosis has been associated with poorer outcomes in tetralogy of Fallot, however only a handful of studies have assessed its significance in the current era. Our aim was to quantify the amount of late gadolinium enhancement in both the LV and RV in a contemporary cohort of adults with surgically repaired tetralogy of Fallot, and assess the relationship with adverse clinical outcomes. Design: Single centre cohort study Setting: National tertiary referral center Patients: One hundred fourteen patients with surgically repaired tetralogy of Fallot with median age 29.5 years (range 17.5-64.2). Prospective follow-up for mean 2.4 years (SD 1.29). Interventions: Cardiovascular magnetic resonance was performed, and late gadolinium enhancement mass was estimated for the LV using the 5-SD remote myocardium method, and for the RV using a segmental scoring system. Cohort characterization was determined through the use of a computerized database. Outcome measures: Survival analysis from time of scan to first adverse event, defined as an episode of atrial arrhythmia, sustained ventricular arrhythmia, hospitalization with heart failure, or implantable cardioverter-defibrillator insertion. Results: Eleven patients experienced an adverse outcome in the follow-up period, although there were no deaths. LV late gadolinium enhancement was associated with adverse outcomes in a univariate model (P = .027). However, when adjusted for age at scan the significant variables included NYHA class (P = .006), peak oxygen uptake (P = .028), number of prior sternotomies (P = .044), and higher indexed RV and LV end diastolic volumes (P = .002 and P < .001), but not RV or LV late gadolinium enhancement. Conclusions: Formal quantification of late gadolinium enhancement is not currently as helpful in ascertaining prognosis compared to other, more easily assessed parameters in a contemporary cohort of tetralogy of Fallot survivors, however assessment particularly of the LV holds promise for the future

Coronary CT Angiography and 5-Year Risk of Myocardial Infarction.

BACKGROUND: Although coronary computed tomographic angiography (CTA) improves diagnostic certainty in the assessment of patients with stable chest pain, its effect on 5-year clinical outcomes is unknown. METHODS: In an open-label, multicenter, parallel-group trial, we randomly assigned 4146 patients with stable chest pain who had been referred to a cardiology clinic for evaluation to standard care plus CTA (2073 patients) or to standard care alone (2073 patients). Investigations, treatments, and clinical outcomes were assessed over 3 to 7 years of follow-up. The primary end point was death from coronary heart disease or nonfatal myocardial infarction at 5 years. RESULTS: The median duration of follow-up was 4.8 years, which yielded 20,254 patient-years of follow-up. The 5-year rate of the primary end point was lower in the CTA group than in the standard-care group (2.3% [48 patients] vs. 3.9% [81 patients]; hazard ratio, 0.59; 95% confidence interval [CI], 0.41 to 0.84; P=0.004). Although the rates of invasive coronary angiography and coronary revascularization were higher in the CTA group than in the standard-care group in the first few months of follow-up, overall rates were similar at 5 years: invasive coronary angiography was performed in 491 patients in the CTA group and in 502 patients in the standard-care group (hazard ratio, 1.00; 95% CI, 0.88 to 1.13), and coronary revascularization was performed in 279 patients in the CTA group and in 267 in the standard-care group (hazard ratio, 1.07; 95% CI, 0.91 to 1.27). However, more preventive therapies were initiated in patients in the CTA group (odds ratio, 1.40; 95% CI, 1.19 to 1.65), as were more antianginal therapies (odds ratio, 1.27; 95% CI, 1.05 to 1.54). There were no significant between-group differences in the rates of cardiovascular or noncardiovascular deaths or deaths from any cause. CONCLUSIONS: In this trial, the use of CTA in addition to standard care in patients with stable chest pain resulted in a significantly lower rate of death from coronary heart disease or nonfatal myocardial infarction at 5 years than standard care alone, without resulting in a significantly higher rate of coronary angiography or coronary revascularization. (Funded by the Scottish Government Chief Scientist Office and others; SCOT-HEART ClinicalTrials.gov number, NCT01149590 .)

Comprehensive Echocardiographic and Cardiovascular Magnetic Resonance Evaluation Differentiates Between Patients with Heart Failure with Preserved Ejection Fraction, Hypertensive Patients and Healthy Controls

Objectives: The aim of this study was to investigate the utility of a comprehensive imaging protocol including echocardiography and cardiac magnetic resonance in the diagnosis and differentiation of hypertensive heart disease and heart failure with preserved ejection fraction (HFpEF). Background: Hypertension is present in up to 90% of patients with HFpEF and is a major etiological component. Despite current recommendations and diagnostic criteria for HFpEF, no noninvasive imaging technique has as yet shown the ability to identify any structural differences between patients with hypertensive heart disease and HFpEF. Methods: We conducted a prospective cross-sectional study of 112 well-characterized patients (62 with HFpEF, 22 with hypertension, and 28 healthy control subjects). All patients underwent cardiopulmonary exercise and biomarker testing and an imaging protocol including echocardiography with speckle-tracking analysis and cardiac magnetic resonance including T1 mapping pre- and post-contrast. Results: Echocardiographic global longitudinal strain (GLS) and extracellular volume (ECV) measured by cardiac magnetic resonance were the only variables able to independently stratify among the 3 groups of patients. ECV was the best technique for differentiation between hypertensive heart disease and HFpEF (ECV area under the curve: 0.88; GLS area under the curve: 0.78; p < 0.001 for both). Using ECV, an optimal cutoff of 31.2% gave 100% sensitivity and 75% specificity. ECV was significantly higher and GLS was significantly reduced in subjects with reduced exercise capacity (lower peak oxygen consumption and higher minute ventilation–carbon dioxide production) (p < 0.001 for both ECV and GLS). Conclusions: Both GLS and ECV are able to independently discriminate between hypertensive heart disease and HFpEF and identify patients with prognostically significant functional limitation. ECV is the best diagnostic discriminatory marker of HFpEF and could be used as a surrogate endpoint for therapeutic studies

Non-invasive assessment of coronary artery disease in patients with left bundle branch block

There is a high prevalence of coronary artery disease (CAD) in patients with left bundle branch block (LBBB); however there are many other causes for this electrocardiographic abnormality. Non-invasive assessment of these patients remains difficult, and all commonly used modalities exhibit several drawbacks. This often leads to these patients undergoing invasive coronary angiography which may not have been necessary. In this review, we examine the uses and limitations of commonly performed non-invasive tests for diagnosis of CAD in patients with LBBB