Prognostic significance of infarct core pathology revealed by quantitative non-contrast in comparison with contrast cardiac magnetic resonance imaging in reperfused ST-elevation myocardial infarction survivors.

AIMS: To assess the prognostic significance of infarct core tissue characteristics using cardiac magnetic resonance (CMR) imaging in survivors of acute ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: We performed an observational prospective single centre cohort study in 300 reperfused STEMI patients (mean ± SD age 59 ± 12 years, 74% male) who underwent CMR 2 days and 6 months post-myocardial infarction (n = 267). Native T1 was measured in myocardial regions of interest (n = 288). Adverse remodelling was defined as an increase in left ventricular (LV) end-diastolic volume ≥20% at 6 months. All-cause death or first heart failure hospitalization was a pre-specified outcome that was assessed during follow-up (median duration 845 days). One hundred and sixty (56%) patients had a hypo-intense infarct core disclosed by native T1. In multivariable regression, infarct core native T1 was inversely associated with adverse remodelling [odds ratio (95% confidence interval (CI)] per 10 ms reduction in native T1: 0.91 (0.82, 0.00); P = 0.061). Thirty (10.4%) of 288 patients died or experienced a heart failure event and 13 of these events occurred post-discharge. Native T1 values (ms) within the hypo-intense infarct core (n = 160 STEMI patients) were inversely associated with the risk of all-cause death or first hospitalization for heart failure post-discharge (for a 10 ms increase in native T1: hazard ratio 0.730, 95% CI 0.617, 0.863; P < 0.001) including after adjustment for left ventricular ejection fraction, infarct core T2 and myocardial haemorrhage. The prognostic results for microvascular obstruction were similar. CONCLUSION: Infarct core native T1 represents a novel non-contrast CMR biomarker with potential for infarct characterization and prognostication in STEMI survivors. Confirmatory studies are warranted. CLINICALTRIALS. GOV IDENTIFIER: NCT02072850.

Contemporary surgical management of infective endocarditis of the aortic root.

Infective endocarditis involving the aortic root is associated with a high degree of morbidity and mortality. Native aortic root infections can develop from aggressive organisms or from delays in diagnosis or definitive care, whereas prosthetic valve infections commonly result in extensive destruction of the aortic root and neighboring structures. Early detection, tailored antibiotic therapy, thoughtful pre-operative planning, and multidisciplinary heart team management are the keys to optimizing patient outcomes. Aggressive and complete surgical debridement are mandatory prior to aortic root reconstruction. Surgical experience and patient-centered decision making are critical in selecting the optimal reconstructive strategy for the aortic root and adjacent structures. Supplementary Information: The online version contains supplementary material available at 10.1007/s12055-023-01604-6.

Corticosteroid and Immunosuppressant Therapy for Cardiac Sarcoidosis: A Systematic Review.

Background Corticosteroid therapy for the treatment of clinically manifest cardiac sarcoidosis is generally recommended. Our group previously systematically reviewed the data in 2013; since then, there has been increasing quality and quantity of data and also interest in nonsteroid agents. Methods and Results Studies were identified from MEDLINE, EMBASE, Cochrane Controlled Trials Register, Cochrane Database of Systematic Reviews, and the National Institutes of Health ClinicalTrials.gov database. The quality of included articles was rated using Scottish Intercollegiate Guidelines Network 50. Outcomes examined were atrioventricular conduction, left ventricular function, ventricular arrhythmias, and mortality. A total of 3527 references were retrieved, and 34 publications met the inclusion criteria. There were no randomized trials, and only 2 studies were rated good quality. In the 34 reports (total of 1297 patients), 1125 patients received corticosteroids, 235 received additional or other immunosuppressant therapy, and 97 patients received no therapy. There were 178 patients treated for atrioventricular conduction disease, with 76/178 (42.7%) improving. In contrast, 21 patients were not treated with corticosteroids and/or immunosuppressant therapy, and none of them improved. Therapy was associated with the prevention of deterioration in left ventricular function. A total of 8 publications reported on ventricular arrhythmia burden, and 19 reported on mortality; the data quality was too limited to draw conclusions for the latter 2 outcomes. Conclusions The best quality data relate to atrioventricular nodal conduction and left ventricular function recovery. In both situations, therapy with corticosteroids and/or immunosuppressant therapy were sometimes associated with positive outcomes. The data quality is too limited to draw conclusions for ventricular arrhythmias and mortality.

Vascular effects of serelaxin in patients with stable coronary artery disease: a randomized placebo-controlled trial.

AIMS: The effects of serelaxin, a recombinant form of human relaxin-2 peptide, on vascular function in the coronary microvascular and systemic macrovascular circulation remain largely unknown. This mechanistic, clinical study assessed the effects of serelaxin on myocardial perfusion, aortic stiffness, and safety in patients with stable coronary artery disease (CAD). METHODS AND RESULTS: In this multicentre, double-blind, parallel-group, placebo-controlled study, 58 patients were randomized 1:1 to 48 h intravenous infusion of serelaxin (30 µg/kg/day) or matching placebo. The primary endpoints were change from baseline to 47 h post-initiation of the infusion in global myocardial perfusion reserve (MPR) assessed using adenosine stress perfusion cardiac magnetic resonance imaging, and applanation tonometry-derived augmentation index (AIx). Secondary endpoints were: change from baseline in AIx and pulse wave velocity, assessed at 47 h, Day 30, and Day 180; aortic distensibility at 47 h; pharmacokinetics and safety. Exploratory endpoints were the effect on cardiorenal biomarkers [N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hsTnT), endothelin-1, and cystatin C]. Of 58 patients, 51 were included in the primary analysis (serelaxin, n = 25; placebo, n = 26). After 2 and 6 h of serelaxin infusion, mean placebo-corrected blood pressure reductions of -9.6 mmHg (P = 0.01) and -13.5 mmHg (P = 0.0003) for systolic blood pressure and -5.2 mmHg (P = 0.02) and -8.4 mmHg (P = 0.001) for diastolic blood pressure occurred. There were no between-group differences from baseline to 47 h in global MPR (-0.24 vs. -0.13, P = 0.44) or AIx (3.49% vs. 0.04%, P = 0.21) with serelaxin compared with placebo. Endothelin-1 and cystatin C levels decreased from baseline in the serelaxin group, and there were no clinically relevant changes observed with serelaxin for NT-proBNP or hsTnT. Similar numbers of serious adverse events were observed in both groups (serelaxin, n = 5; placebo, n = 7) to 180-day follow-up. CONCLUSION: In patients with stable CAD, 48 h intravenous serelaxin reduced blood pressure but did not alter myocardial perfusion.

Comparing and Contrasting Guidelines for the Management of Cardiac Sarcoidosis.

Introduction: The Japanese Circulation Society (JCS) recently published new guidelines for the diagnosis and treatment of Cardiac Sarcoidosis (CS). There are two other guideline documents, the World Association of Sarcoidosis and Other Granulomatous Disorders Sarcoidosis Organ (WASOG) Assessment Instrument created in 1999 and updated in 2014. Also, in 2014, the Heart Rhythm Society (HRS) published their international guideline document. As co-chair of the HRS document I have been invited to compare and contrast the management aspects of the HRS guidelines with the new JCS document. Comments: (i) The HRS document recommended a stepwise approach to VT management and the JCS document is somewhat similar; but with some key differences. (ii) The HRS statement suggested that an ICD for CS patients with an indication for a pacemaker "can be useful". The JCS document take a similar position although with some additional criteria related to National Health Institute Coverage guidelines. (iii) Both HRS and the JCS documents agree that ICDs are recommended in patients with general guideline indications for primary prevention (i.e. LVEF less than 35%). However which additional patients should be considered for ICDs is controversial. The 2016 JCS document is broadly similar, with the major exception that it is recommended that all patients with LVEF 35-50% should have an EP study. Conclusion: The Japanese have been leaders in many aspects of CS including in guideline development. It is clear that the future of CS management is bright, with increasing international collaborations and also multiple efforts underway to obtain higher quality data to inform future guidelines.

Pathophysiology of LV Remodeling in Survivors of STEMI: Inflammation, Remote Myocardium, and Prognosis.

OBJECTIVES: The aim of this study was to investigate the clinical significance of native T1 values in remote myocardium in survivors of acute ST-segment elevation myocardial infarction (STEMI). BACKGROUND: The pathophysiology and prognostic significance of remote myocardium in the natural history of STEMI is uncertain. Cardiac magnetic resonance (CMR) reveals myocardial function and pathology. Native T1 (relaxation time in ms) is a fundamental magnetic resonance tissue property determined by water content and cellularity. RESULTS: A total of 300 STEMI patients (mean age 59 years; 74% male) gave informed consent. A total of 288 STEMI patients had evaluable native T1 CMR, and 267 patients (91%) had follow-up CMR at 6 months. Health outcome information was obtained for all of the participants (median follow-up 845 days). Infarct size was 18 ± 13% of left ventricular (LV) mass. Two days post-STEMI, native T1 was lower in remote myocardium than in the infarct zone (961 ± 25 ms vs. 1,097 ± 52 ms; p < 0.01). In multivariable regression, incomplete ST-segment resolution was associated with myocardial remote zone native T1 (regression coefficient 9.42; 95% confidence interval [CI]: 2.37 to 16.47; p = 0.009), as were the log of the admission C-reactive protein concentration (3.01; 95% CI: 0.016 to 5.85; p = 0.038) and the peak monocyte count (10.20; 95% CI: 0.74 to 19.67; p = 0.035). Remote T1 at baseline was associated with log N-terminal pro-B-type natriuretic peptide at 6 months (0.01; 95% CI: 0.00 to 0.02; p = 0.002; n = 151) and the change in LV end-diastolic volume from baseline to 6 months (0.13; 95% CI: 0.01 to 0.24; p = 0.035). Remote zone native T1 was independently associated with post-discharge major adverse cardiac events (n = 20 events; hazard ratio: 1.016; 95% CI: 1.000 to 1.032; p = 0.048) and all-cause death or heart failure hospitalization (n = 30 events during admission and post-discharge; hazard ratio: 1.014; 95% CI: 1.000 to 1.028; p = 0.049). CONCLUSIONS: Reperfusion injury and inflammation early post-MI was associated with remote zone T1, which in turn was independently associated with LV remodeling and adverse cardiac events post-STEMI. (Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction [BHF MR-MI]; NCT02072850).

Microvascular Resistance Predicts Myocardial Salvage and Infarct Characteristics in ST-Elevation Myocardial Infarction.

BACKGROUND: 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. METHODS AND RESULTS: 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. T(2)-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. CONCLUSION: 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. (J Am Heart Assoc. 2012;1:e002246 doi: 10.1161/JAHA.112.002246).

Bright-blood T2-weighted MRI has higher diagnostic accuracy than dark-blood short tau inversion recovery MRI for detection of acute myocardial infarction and for assessment of the ischemic area at risk and myocardial salvage.

BACKGROUND: T2-Weighted MRI reveals myocardial edema and enables estimation of the ischemic area at risk and myocardial salvage in patients with acute myocardial infarction (MI). We compared the diagnostic accuracy of a new bright-blood T2-weighted with a standard black blood T2-weighted MRI in patients with acute MI. METHODS AND RESULTS: A breath-hold, bright-blood T2-weighted, Acquisition for Cardiac Unified T2 Edema pulse sequence with normalization for coil sensitivity and a breath-hold T2 dark-blood short tau inversion recovery sequence were used to depict the area at risk in 54 consecutive acute MI patients. Infarct size was measured on gadolinium late contrast enhancement images. Compared with dark-blood T2-weighted MRI, consensus agreements between independent observers for identification of myocardial edema were higher with bright-blood T2-weighted MRI when evaluated per patient (P<0.001) and per segment of left ventricle (P<0.001). Compared with bright-blood T2-weighted MRI, dark-blood T2-weighted MRI underestimated the area at risk compared with infarct size (P<0.001). The 95% limits of agreement for interobserver agreements for the ischemic area at risk and myocardial salvage were wider with dark-blood T2-weighted MRI than with bright-blood T2-weighted MRI. Bright blood enabled more accurate identification of the culprit coronary artery with correct identification in 94% of cases compared with 61% for dark blood (P<0.001). CONCLUSIONS: Bright-blood T2-weighted MRI has higher diagnostic accuracy than dark-blood T2-weighted MRI. Additionally, dark-blood T2-weighted MRI may underestimate area at risk and myocardial salvage.