Acute coronary occlusion after surgical replacement of the aortic valve treated with emergency off-pump coronary artery bypass grafting.

Acute coronary occlusion after surgical replacement of the aortic valve is a rare but potentially fatal event. Due to its rarity, there is no univocal treatment with the percutaneous approach being the most commonly used for its promptness and ease of use. Only a few cases have been treated with coronary artery bypass grafting (CABG) and, to the best of our knowledge, none has been reported with the use of off-pump CABG (OPCABG). Here we describe the case of acute coronary occlusion of the circumflex artery immediately after surgical replacement of the aortic valve in a 79-year-old patient. The occlusion was promptly diagnosed and treated with interval emergency balloon angioplasty followed by OPCABG of the circumflex artery. The patient made a full recovery and was discharged home 12 days after the surgery.

Long-term outcome of myocardial scarring and deformation with cardiovascular magnetic resonance in out of hospital cardiac arrest survivors.

AIMS: Cardiovascular magnetic resonance (CMR) is increasingly recognized as a diagnostic and prognostic tool in out of hospital cardiac arrest (OHCA) survivors. After assessing CMR findings early after ventricular fibrillation (VF) OHCA, we sought to explore the long-term outcome of myocardial scarring and deformation. METHODS AND RESULTS: We included 121 consecutive VF OHCA survivors (82% male, median 62 years) undergoing CMR within 2 weeks from cardiac arrest. Late gadolinium-enhancement (LGE) was quantified using the full width at half maximum method and tissue tracking analysis software was used to assess myocardial deformation. LGE was found in 71% of patients (median LGE mass 6.2% of the left ventricle, LV), mainly with an ischaemic pattern. Myocardial deformation was overall impaired and showed a significant correlation with LGE presence and extent (P < 0.001). A composite end-point of all-cause mortality and appropriate ICD discharge/anti-tachycardia pacing was met in 24% of patients. Patients meeting the end-point had significantly greater LGE extent (8.6% of LV myocardium vs. 4.1%, P = 0.02), while there was no difference with regards to myocardial deformation. Survival rate was significantly lower in patients with LGE (P = 0.05) and LGE mass >4.4% of the LV identified a group of patients at higher risk of adverse events (P = 0.005). CONCLUSIONS: We found a high prevalence of LGE, early after OHCA, and an overall impaired myocardial deformation. On long-term follow-up both LGE presence and extent showed a significant association with recurrent adverse events, while LV ejection fraction and myocardial deformation did not identify patients with an unfavourable outcome.

Beyond apical ballooning: computational modelling reveals morphological features of Takotsubo cardiomyopathy.

Takotsubo cardiomyopathy (TCM) is characterized by transient myocardial dysfunction, typically at the left ventricular (LV) apex. Its pathophysiology and recovery mechanisms remain unknown. We investigated LV morphology and deformation in n = 28 TCM patients. Patients with MRI within 5 days from admission ("early TCM") showed reduced LVEF and higher ventricular volumes, but no differences in ECG, global strains or myocardial oedema. Statistical shape modelling described LV size (Mode 1), apical sphericity (Mode 2) and height (Mode 3). Significant differences in Mode 1 suggest that "early TCM" LV remodeling is mainly influenced by a change in ventricular size rather than apical sphericity.

Prognostic Role of CMR and Conventional Risk Factors in Myocardial Infarction With Nonobstructed Coronary Arteries.

OBJECTIVES: This study sought to assess the prognostic impact of cardiac magnetic resonance (CMR) and conventional risk factors in patients with myocardial infarction with nonobstructed coronaries (MINOCA). BACKGROUND: Myocardial infarction with nonobstructed coronary arteries (MINOCA) represents a diagnostic dilemma, and the prognostic markers have not been clarified. METHODS: A total of 388 consecutive patients with MINOCA undergoing CMR assessment were identified retrospectively from a registry database and prospectively followed for a primary clinical endpoint of all-cause mortality. A 1.5-T CMR was performed using a comprehensive protocol (cines, T2-weighted, and late gadolinium enhancement sequences). Patients were grouped into 4 categories based on their CMR findings: myocardial infarction (MI) (embolic/spontaneous recanalization), myocarditis, cardiomyopathy, and normal CMR. RESULTS: CMR (performed at a median of 37 days from presentation) was able to identify the cause for the troponin rise in 74% of the patients (25% myocarditis, 25% MI, and 25% cardiomyopathy), whereas a normal CMR was identified in 26%. Over a median follow-up of 1,262 days (3.5 years), 5.7% patients died. The cardiomyopathy group had the worst prognosis (mortality 15%; log-rank test: 19.9; p < 0.001), MI had 4% mortality, and 2% in both myocarditis and normal CMR. In a multivariable Cox regression model (including clinical and CMR parameters), CMR diagnosis of cardiomyopathy and ST-segment elevation on presentation electrocardiogram (ECG) remained the only 2 significant predictors of mortality. Using presentation with ECG ST-segment elevation and CMR diagnosis of cardiomyopathy as risk markers, the mortality risk rates were 2%, 11%, and 21% for presence of 0, 1, and 2 factors, respectively (p < 0.0001). CONCLUSIONS: In a large cohort of patients with MINOCA, CMR (median 37 days from presentation) identified a final diagnosis in 74% of patients. Cardiomyopathy had the highest mortality, followed by MI. The strongest predictors of mortality were a CMR diagnosis of cardiomyopathy and ST-segment elevation on presentation ECG.

Left ventricular extracellular volume fraction and atrioventricular interaction in hypertension.

OBJECTIVES: Left atrial enlargement (LAE) predicts cardiovascular morbidity and mortality. Impaired LA function also confers poor prognosis. This study aimed to determine whether left ventricular (LV) interstitial fibrosis is associated with LAE and LA impairment in systemic hypertension. METHODS: Following informed written consent, a prospective observational study of 86 hypertensive patients (49 ± 15 years, 53% male, office SBP 168 ± 30 mmHg, office DBP 97 ± 4 mmHg) and 20 normotensive controls (48 ± 13 years, 55% male, office SBP 130 ± 13 mmHg, office DBP 80 ± 11 mmHg) at 1.5-T cardiovascular magnetic resonance was conducted. Extracellular volume fraction (ECV) was calculated by T1-mapping. LA volume (LAV) was measured with biplane area-length method. LA reservoir, conduit and pump function were calculated with the phasic volumetric method. RESULTS: Indexed LAV correlated with indexed LV mass (R = 0.376, p < 0.0001) and ECV (R = 0.359, p = 0.001). However, ECV was the strongest significant predictor of LAE in multivariate regression analysis (odds ratio [95th confidence interval] 1.24 [1.04-1.48], p = 0.017). Indexed myocardial interstitial volume was associated with significant reductions in LA reservoir (R = -0.437, p < 0.0001) and conduit (R = -0.316, p = 0.003) but not pump (R = -0.167, p = 0.125) function. Multiple linear regression, correcting for age, gender, BMI, BP and diabetes, showed an independent decrease of 3.5% LA total emptying fraction for each 10 ml/m2 increase in myocardial interstitial volume (standard ß coefficient -3.54, p = 0.002). CONCLUSIONS: LV extracellular expansion is associated with LAE and impaired LA reservoir and conduit function. Future studies should identify if targeting diffuse LV fibrosis is beneficial in reverse remodelling of LA structural and functional pathological abnormalities in hypertension. KEY POINTS: • Left atrial enlargement (LAE) and impairment are markers of adverse prognosis in systemic hypertension but their pathophysiology is poorly understood. • Left ventricular extracellular volume fraction was the strongest independent multivariate predictor of LAE and was associated with impaired left atrial reservoir and conduit function. • LV interstitial expansion may play a central role in the pathophysiology of adverse atrioventricular interaction in systemic hypertension.

Native T1 mapping to detect extent of acute and chronic myocardial infarction: comparison with late gadolinium enhancement technique.

Investigate whether native-T1 mapping can assess the transmural extent of myocardial infarction (TEI) thereby differentiating viable from non-viable myocardium without the use of gadolinium-contrast in both acute and chronic myocardial infarction (aMI and cMI). Sixty patients (30 cMI > 1 year and 30 aMI day 2 STEMI) and 20 healthy-controls underwent 1.5 T CMR to assess left ventricular function (cine), native-T1 mapping (MOLLI sequence 5(3)3, motion-corrected) and the presence and TEI from late gadolinium enhancement (LGE) images. Segments with TEI > 75% was considered non-viable. Gold-standard LGE-TEI was compared with corresponding segmental native-T1. Segmental native-T1 correlated significantly with TEI (R = 0.74, p < 0.001 in cMI and R = 0.57, p < 0.001 in aMI). Native-T1 differentiated segments with no LGE (1031 ± 31 ms), LGE positive but viable (1103 ± 57 ms) and LGE positive but non-viable (1206 ± 118 ms) in cMI (p < 0.01). It also differentiated segments with no LGE (1054 ± 65 m), LGE positive but viable (1135 ± 73 ms) and LGE positive but non-viable (1168 ± 71 ms) in aMI (p < 0.01). ROC analysis demonstrated excellent accuracy of native-T1 mapping compared to LGE-TEI (AUC - 0.88, p < 0.001 in cMI, vs AUC - 0.83, p < 0.001 in aMI). Native-T1 performed better in cMI than aMI (p < 0.01). In cMI a segmental T1 threshold of 1085 ms differentiated viable from non-viable segments with a sensitivity 88% and specificity of 88% whereas a T1 of 1110 ms differentiated viable from nonviable with 79% sensitivity and 79% specificity in aMI. Native-T1 mapping correlates significantly with TEI thereby differentiating between normal, viable, and non-viable myocardium with distinctive T1 profiles in aMI and cMI. Native T1-mapping to detect MI performed better in cMI compared to aMI due to absence of myocardial oedema. Native-T1 mapping holds promise for viability assessment without the need for gadolinium-contrast agent.

Cardiac biomarkers of acute coronary syndrome: from history to high-sensitivity cardiac troponin.

The role of cardiac troponins as diagnostic biomarkers of myocardial injury in the context of acute coronary syndrome (ACS) is well established. Since the initial 1st-generation assays, 5th-generation high-sensitivity cardiac troponin (hs-cTn) assays have been developed, and are now widely used. However, its clinical adoption preceded guidelines and even best practice evidence. This review summarizes the history of cardiac biomarkers with particular emphasis on hs-cTn. We aim to provide insights into using hs-cTn as a quantitative marker of cardiomyocyte injury to help in the differential diagnosis of coronary versus non-coronary cardiac diseases. We also review the recent evidence and guidelines of using hs-cTn in suspected ACS.

The Relationship Between Left Ventricular Wall Thickness, Myocardial Shortening, and Ejection Fraction in Hypertensive Heart Disease: Insights From Cardiac Magnetic Resonance Imaging.

Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age- and sex-matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long-axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end-diastolic wall thickness increased. However, absolute wall thickening (defined as end-systolic minus end-diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted ß-coefficient: 3.43 [2.60-4.26], P<.0001). Increasing end-diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy.

Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes.

OBJECTIVE: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR). METHODS: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements. RESULTS: 88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m(2) vs concentric LVH: 73±15 mL/m(2) vs concentric remodelling: 55±9 mL/m(2), p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m(2) vs concentric LVH: 30±10 mL/m(2) vs concentricremodelling: 19±2 mL/m(2), p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: -12.8±4.6% vs concentric LVH: -15.5±3.1% vs concentric remodelling: -17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls. CONCLUSIONS: Myocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments.

Extra-cardiac findings in cardiovascular magnetic resonance: what the imaging cardiologist needs to know.

Cardiovascular magnetic resonance (CMR) is an established non-invasive technique to comprehensively assess cardiovascular structure and function in a variety of acquired and inherited cardiac conditions. A significant amount of the neck, thorax and upper abdomen are imaged at the time of routine clinical CMR, particularly in the initial multi-slice axial and coronal images. The discovery of unsuspected disease at the time of imaging has ethical, financial and medico-legal implications. Extra-cardiac findings at the time of CMR are common, can be important and can change clinical management. Certain patient groups undergoing CMR are at particular risk of important extra-cardiac findings as several of the cardiovascular risk factors for atherosclerosis are also risk factors for malignancy. Furthermore, the presence of certain extra-cardiac findings may contribute to the interpretation of the primary cardiac pathology as some cardiac conditions have multi-systemic extra-cardiac involvement. The aim of this review is to give an overview of the type of extra-cardiac findings that may become apparent on CMR, subdivided by anatomical location. We focus on normal variant anatomy that may mimic disease, common incidental extra-cardiac findings and important imaging signs that help distinguish sinister pathology from benign disease. We also aim to provide a framework to the approach and potential further diagnostic work-up of incidental extra-cardiac findings discovered at the time of CMR. However, it is beyond the scope of this review to discuss and determine the clinical significance of extracardiac findings at CMR.

Additional value of Galectin-3 to BNP in acute heart failure patients with preserved ejection fraction.

BACKGROUND: Almost half of patients with acute heart failure have preserved ejection fraction (HFpEF). HFpEF is a diagnostic challenge using traditional investigation tools; Galectin-3 (Gal-3) is an emerging biomarker useful in individuals at risk for HF. The aim of our study is to analyse the relation and prognostic value of Gal-3, BNP and renal dysfunction in patients with HFpEF compared to patients with reduced ejection fraction (HFrEF). METHODS: We enrolled 98 patients with acute heart failure (AHF) and measured Gal-3, BNP, and estimated glomerular filtration rate (eGFR) within 12h of hospital admission. On the basis of echocardiographic findings we divided our sample into two groups: patients with HFrHF (ejection fraction<50%) or HFpEF (ejection fraction>50%). Patients were followed up at 6months. RESULTS: No differences in Gal-3 levels were found in the two subgroups (HFrEF: 19.5±5.1ng/mL; HFpEF: 20.5±8.7, p=0.56). Gal-3 was inversely related to renal dysfunction (LogGal-3 vs eGFR: r=-0.30, p=0.01) but did not correlate with LogBNP levels (r=0.07, p=0.55). Gal-3 was associated with more advanced diastolic dysfunction in HFpEF (p=0.009). In addition LogGal-3 was related to diastolic LV stiffness (all patients: r=0.45, p<0.001; HFpEF: r=0.64, p<0.001). Cox regression analysis showed that LogGal-3>1.30 was related to poor outcome independently from renal dysfunction and other risk factors only in HFpEF (univariate HR 23.98 [3.03-89.45]; p<0.001). Adjusted for renal dysfunction (HR 16.32 [1.98-34.09]; p=0.009). CONCLUSIONS: Gal-3 is not able to distinguish between HFrEF and HFpEF patients. However it is related to diastolic dysfunction severity and LV stiffness in HFpEF. Gal-3 demonstrates a prognostic role independently from renal dysfunction in subjects with HFpEF.

Prevalence and predictors of asymmetric hypertensive heart disease: insights from cardiac and aortic function with cardiovascular magnetic resonance.

AIMS: We sought to determine the prevalence of asymmetric hypertensive heart disease (HHD) overlapping morphologically with hypertrophic cardiomyopathy (HCM) and to determine predictors of this pattern of hypertensive remodelling. METHODS AND RESULTS: One hundred and fifty hypertensive patients underwent 1.5 T cardiovascular magnetic resonance imaging. Twenty-one patients were excluded due to concomitant cardiac pathology that may confound the hypertrophic response, e.g. myocardial infarction, moderate-severe valvular disease, or other cardiomyopathy. Asymmetric HHD was defined as a segmental wall thickness of ≥15 mm and >1.5-fold the opposing wall in ≥1 myocardial segments, measured from short-axis cine stack at end-diastole. Ambulatory blood pressure, myocardial replacement fibrosis, aortic distensibility and aortoseptal angle were investigated as predictors of asymmetric HHD by multivariate logistic regression. Out of 129 hypertensive subjects (age: 51 ± 15 years, 50% male, systolic blood pressure: 170 ± 30 mmHg, diastolic blood pressure: 97 ± 16 mmHg), asymmetric HHD occurred in 21%. Where present, maximal end-diastolic wall thickness (EDWT) was 17.8 ± 1.9 mm and located exclusively in the basal or mid septum. In asymmetric HHD, aortoseptal angle (114 ± 10° vs. 125 ± 9° vs. 123 ± 12°, P < 0.05, respectively) was significantly reduced compared to concentric left ventricular hypertrophy (LVH) and compared to no LVH, respectively. Aortic distensibility in asymmetric HHD (1.01 ± 0.60 vs. 1.83 ± 1.65 mm2/mmHg × 103, P < 0.05, respectively) was significantly reduced compared to subjects with no LVH. Age (odds ratio [95th confidence interval]: 1.10 [1.02-1.18], P < 0.05) and indexed LV mass (1.09 [0.98-1.28], P < 0.0001) were significant, independent predictors of asymmetric HDD. CONCLUSIONS: Asymmetric HHD morphologically overlapping with HCM, according to the current ESC guidelines, is common. Postulating a diagnosis of HCM on the basis of EDWT of ≥15 mm should be made with caution in the presence of arterial hypertension particular in male subjects with elevated LV mass.

The Role of Cardiac MRI in Patients with Troponin-Positive Chest Pain and Unobstructed Coronary Arteries.

Acute coronary syndrome (ACS) still remains one of the leading causes of mortality and morbidity worldwide. Seven to fifteen percent of patients presenting with ACS have unobstructed coronary artery disease (CAD) on urgent angiography. Patients with ACS and unobstructed coronary arteries represent a clinical dilemma and their diagnosis and management is quite variable in current practice. Cardiovascular magnetic resonance imaging with its unique non-invasive myocardial tissue characterization property has the potential to identify underlying etiologies and reach a final diagnosis. These include acute and chronic myocarditis, embolic/spontaneous recanalization myocardial infarction, and Tako-Tsubo cardiomyopathy, and other conditions. Establishing a final diagnosis has a direct implication on patient's management and prognosis. In this article, we have reviewed the current evidence on the diagnostic role of cardiac magnetic resonance (CMR) in patients with ACS and unobstructed coronary arteries. We have also highlighted the potential role of CMR as a risk stratification or prognostication tool for this patient population.