Sex-specific ventricular morphology, function, and tissue characteristics in arterial hypertension: a magnetic resonance study of the Hamburg city health cohort.

OBJECTIVE: To determine the influence of arterial hypertension (AHT), sex, and the interaction between both left- and right ventricular (LV, RV) morphology, function, and tissue characteristics. METHODS: The Hamburg City Health Study (HCHS) is a population-based, prospective, monocentric study. 1972 individuals without a history of cardiac diseases/ interventions underwent 3 T cardiac MR imaging (CMR). Generalized linear models were conducted, including AHT, sex (and the interaction if significant), age, body mass index, place of birth, diabetes mellitus, smoking, hyperlipoproteinemia, atrial fibrillation, and medication. RESULTS: Of 1972 subjects, 68% suffered from AHT. 42% with AHT and 49% controls were female. Females overall showed a higher ejection fraction (EF) (LV: regression coefficient +2.4% [95% confidence interval: 1.7; 3.1]), lower volumes and LV mass (-19.8% [-21.3; -18.5]), and prolonged native septal T1 (+22.1 ms [18.3; 25.9])/T2 relaxation times (+1.1 ms [0.9; 1.3]) (all p < 0.001) compared to males. Subjects with AHT showed a higher EF (LV: +1.2% [0.3; 2.0], p = 0.009) and LV mass (+6.6% [4.3; 9.0], p < 0.001) than controls. The interaction between sex and AHT influenced mapping. After excluding segments with LGE, males (-0.7 ms [-1.0; -0.3 | ) and females with AHT (-1.1 ms [-1.6; -0.6]) showed shorter T2 relaxation times than the sex-respective controls (p < 0.001), but the effect was stronger in females. CONCLUSION: In the HCHS, female and male subjects with AHT likewise showed a higher EF and LV mass than controls, independent of sex. However, differences in tissue characteristics between subjects with AHT and controls appeared to be sex-specific. CLINICAL RELEVANCE STATEMENT: The interaction between sex and cardiac risk factors is an underestimated factor that should be considered when comparing tissue characteristics between hypertensive subjects and controls, and when establishing cut-off values for normal and pathological relaxation times. KEY POINTS: There are sex-dependent differences in arterial hypertension, but it is unclear if cardiac MR parameters are sex-specific. Differences in cardiac MR parameters between hypertensive subjects and healthy controls appeared to be sex-specific for tissue characteristics. Sex needs to be considered when comparing tissue characteristics in patients with arterial hypertension to healthy controls.

Unrecognized myocardial scar by late-gadolinium-enhancement cardiovascular magnetic resonance: Insights from the population-based Hamburg City Health Study.

BACKGROUND: The presence of myocardial scar is associated with poor prognosis in several underlying diseases. Late-gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging reveals clinically silent "unrecognized myocardial scar" (UMS), but the etiology of UMS often remains unclear. This population-based CMR study evaluated prevalence, localization, patterns, and risk factors of UMS. METHODS: The study population consisted of 1064 consecutive Hamburg City Health Study participants without a history of coronary heart disease or myocarditis. UMS was assessed by standard-phase-sensitive-inversion-recovery LGE CMR. RESULTS: Median age was 66 [quartiles 59, 71] years and 37% (388/1064) were females. UMS was detected in 244 (23%) participants. Twenty-five participants (10%) had ischemic, and 217 participants (89%) had non-ischemic scar patterns, predominantly involving the basal inferolateral left-ventricular (LV) myocardium (75%). Two participants (1%) had coincident ischemic and non-ischemic scar. The presence of any UMS was independently associated with LV ejection fraction (odds ratios (OR) per standard deviation (SD) 0.77 (confidence interval (CI) 0.65-0.90), p = 0.002) and LV mass (OR per SD 1.54 (CI 1.31-1.82), p < 0.001). Ischemic UMS was independently associated with LV ejection fraction (OR per SD 0.58 (CI 0.39-0.86), p = 0.007), LV mass (OR per SD 1.74 (CI 1.25-2.45), p = 0.001), and diabetes (OR 4.91 (CI 1.66-13.03), p = 0.002). Non-ischemic UMS was only independently associated with LV mass (OR per SD 1.44 (CI 1.24-1.69), p < 0.001). CONCLUSION: UMS, in particular with a non-ischemic pattern, is frequent in individuals without known cardiac disease and predominantly involves the basal inferolateral LV myocardium. Presence of UMS is independently associated with a lower LVEF, a higher LV mass, and a history of diabetes.

Prognostic Relevance of Ischemic Late Gadolinium Enhancement in Apparently Healthy Endurance Athletes: A Follow-up Study Over 5 years.

BACKGROUND: In many cardiac diseases, myocardial scar tissue detected by late gadolinium enhancement (LGE) is a risk factor for cardiac arrhythmia and sudden cardiac death. Previous studies in athletes reported an increased risk for cardiac events in this group of ostensibly healthy subjects. However, the currently available longitudinal studies on this topic included fairly old marathon runners with a mean age of 57 ± 6 years or represent a case-control study in athletes with preexisting ventricular arrhythmia. The purpose of this prospective study was to analyze the prognostic relevance of LGE cardiac magnetic resonance (CMR) in middle-aged endurance athletes without known preexisting cardiac disorders. METHODS: Three-hundred and twelve apparently healthy athletes were prospectively enrolled. Inclusion criteria were a training for a minimum of 10 h per week and regularly participation in competitions. LGE CMR was obtained at baseline in all athletes and presence of LGE was classified visually according to established criteria as ischemic LGE, major or minor non-ischemic LGE or absent LGE. Follow-up consisted of a standardized questionnaire and an additional phone call in case of incomplete data. An event was defined as fatal myocardial infarction, ventricular tachycardia, ventricular fibrillation or sudden cardiac death (SCD). RESULTS: Complete follow-up was available for 293/312 athletes (94%) including 145 triathletes, 74 marathon runners and 74 cyclists after a median of 5.6 [quartiles 4,3, 6,4] years. Median age was 44 [35, 50] years at study enrollment. Spiroergometry did not reveal heart rhythm disturbances or significant ECG changes in the study population. LGE CMR revealed myocardial scar/focal fibrosis in 80 of 293 athletes (27%) including 7 athletes (2%) with ischemic subendocardial LGE of the left ventricle (LV), 16 athletes (6%) with major non-ischemic LGE of the LV and 57 athletes (19%) with minor non-ischemic LGE. During follow-up, two athletes experienced SCD. One marathon runner died during a training run and one cyclist died suddenly at rest. Both athletes had ischemic LGE of the LV. The event rate for SCD was 0.7% in the entire study population and 28% in the 7 athletes with ischemic LGE (p < 0.001 compared to athletes without LGE). CONCLUSIONS: Our findings indicate that athletes with ischemic LGE due to unrecognized myocardial infarction are at increased risk for SCD. Our findings highlight the value of LGE CMR to detect occult ischemic scar in asymptomatic apparently healthy athletes, which is of importance, since current guidelines do not recommend to incorporate routine cardiac imaging in pre-participation screening. Athletes with ischemic myocardial scar should at least consider to refrain from high-level exercise as an individual decision.

Contrast-enhanced cardiac MRI is superior to non-contrast mapping to predict left ventricular remodeling at 6 months after acute myocardial infarction.

OBJECTIVES: Parametric mapping constitutes a novel cardiac magnetic resonance (CMR) technique enabling quantitative assessment of pathologic alterations of left ventricular (LV) myocardium. This study aimed to investigate the clinical utility of mapping techniques with and without contrast agent compared to standard CMR to predict adverse LV remodeling following acute myocardial infarction (AMI). MATERIALS AND METHODS: A post hoc analysis was performed on sixty-four consecutively enrolled patients (57 ± 12 years, 54 men) with first-time reperfused AMI. Baseline CMR was obtained at 8 ± 5 days post-AMI, and follow-up CMR at 6 ± 1.4 months. T1/T2 mapping, T2-weighted, and late gadolinium enhancement (LGE) acquisitions were performed at baseline and cine imaging was used to determine adverse LV remodeling, defined as end-diastolic volume increase by 20% at 6 months. RESULTS: A total of 11 (17%) patients developed adverse LV remodeling. At baseline, patients with LV remodeling showed larger edema (30 ± 11 vs. 22 ± 10%LV; p < 0.05), infarct size (24 ± 11 vs. 14 ± 8%LV; p < 0.001), extracellular volume (ECVinfarct; 63 ± 12 vs. 47 ± 11%; p < 0.001), and native T2infarct (95 ± 16 vs. 78 ± 17 ms; p < 0.01). ECVinfarct and infarct size by LGE were the best predictors of LV remodeling with areas under the curve (AUCs) of 0.843 and 0.789, respectively (all p < 0.01). Native T1infarct had the lowest AUC of 0.549 (p = 0.668) and was inferior to edema size by T2-weighted imaging (AUC = 0.720; p < 0.05) and native T2infarct (AUC = 0.766; p < 0.01). CONCLUSION: In this study, ECVinfarct and infarct size by LGE were the best predictors for the development of LV remodeling within 6 months after AMI, with a better discriminative performance than non-contrast mapping CMR. CLINICAL RELEVANCE STATEMENT: This study demonstrates the predictive value of contrast-enhanced and non-contrast as well as conventional and novel CMR techniques for the development of LV remodeling following AMI, which might help define precise CMR endpoints in experimental and clinical myocardial infarction trials. KEY POINTS: • Multiparametric CMR provides insights into left ventricular remodeling at 6 months following an acute myocardial infarction. • Extracellular volume fraction and infarct size are the best predictors for adverse left ventricular remodeling. • Contrast-enhanced T1 mapping has a better predictive performance than non-contrast standard CMR and T1/T2 mapping.

Prevalence and pattern of focal and potential diffuse myocardial fibrosis in male and female marathon runners using contrast-enhanced cardiac magnetic resonance.

OBJECTIVES: This study analyzed the prevalence and pattern of focal and potential diffuse myocardial fibrosis detected by late gadolinium enhancement (LGE) and extracellular volume (ECV) imaging in male and female marathon runners using cardiac magnetic resonance (CMR). METHODS: Seventy-four marathon runners were studied including 55 males (44 ± 8 years) and 19 females (36 ± 7 years) and compared to 36 controls with similar age and sex using contrast-enhanced CMR, exercise testing, and blood samples. RESULTS: Contrast-enhanced CMR revealed focal myocardial fibrosis in 8 of 74 runners (11%). The majority of runners were male (7 of 8, 88%). LGE was typically non-ischemic in 7 of 8 runners (88%) and ischemic in one runner. ECV was higher in remote myocardium without LGE in male runners (25.5 ± 2.3%) compared to male controls (24.0 ± 3.0%, p < 0.05), indicating the potential presence of diffuse myocardial fibrosis. LV mass was higher in LGE + males (86 ± 18 g/m2) compared to LGE- males (73 ± 14 g/m2, p < 0.05). Furthermore, LGE + males had lower weight (69 ± 9 vs 77 ± 9 kg, p < 0.05) and shorter best marathon finishing times (3.2 ± 0.3 h) compared to LGE- males (3.6 ± 0.4 h, p < 0.05) suggesting higher training load in these runners to accomplish the marathon in a short time. CONCLUSION: The high frequency of non-ischemic myocardial fibrosis in LGE + male runners can be related to increased LV mass in these runners. Furthermore, a higher training load could explain the higher LV mass and could be one additional cofactor in the genesis of myocardial fibrosis in marathon runners. KEY POINTS: • A high frequency of myocardial fibrosis was found in marathon runners. • Myocardial fibrosis occurred typically in male runners and was typically non-ischemic. • Higher training load could be one cofactor in the genesis of myocardial fibrosis in marathon runners.

Left ventricular diastolic filling patterns in competitive triathletes with and without myocardial fibrosis by cardiac magnetic resonance time-volume analysis.

PURPOSE: To investigate the influence of myocardial fibrosis on left ventricular (LV) diastolic filling patterns in triathletes compared to sedentary controls by cardiac magnetic resonance (CMR) imaging. METHOD: 101 male triathletes (43 ± 11 years) and 28 controls (41 ± 10 years) were recruited and underwent 1.5 T CMR including cine SSFP series, late gadolinium enhancement (LGE) imaging and T1 mapping. Functional and morphological parameters were obtained, and CMR-based LV diastolic filling parameters such as the early peak-filling rate (EPFR), atrial peak-filling rate (APFR) and peak-filling rate ratio (PFRR = EPFR/APFR) were determined by time-volume analysis of the cine series. RESULTS: Non-ischemic LGE was detected in 20 triathletes (20 %) and in none of the controls. Compared to controls LGE-negative (LGE-) triathletes showed similar EPFR (216 ± 58 ml/s/m2 vs 224 ± 69 ml/s/m2, P = 0.52) but lower APFR (120 ± 46 ml/s/m2 vs 147 ± 55 ml/s/m2, P < 0.05), resulting in higher PFRR (2.1 ± 1 vs 1.6 ± 0.5, P < 0.01). LGE-positive (LGE + ) triathletes had similar EPFR (212 ± 73 ml/s/m2, P = 0.798), but higher APFR (149 ± 50 ml/s/m2, P < 0.05) and decreased PFRR (1.6 ± 0.7, P < 0.05) compared to LGE- triathletes. LGE + triathletes had increased LV mass index (88 ± 10 g/m2 vs 80 ± 12 g/m2, P < 0.01) and extracellular volume (ECV) fraction (26.2 ± 2.7 % vs 24.4 ± 1.7 %, P < 0.001) compared to LGE- triathletes. CONCLUSIONS: Athletic activity leads to "supernormal" LV diastolic filling pattern in LGE- triathletes, which may be attributable to increased LV myocardial flexibility and elasticity. However, LGE + triathletes demonstrate a pseudo-normalization characterized by compensatory increase of atrial contraction. Possibly, due to reduced passive elasticity associated myocardial fibrosis.

Cardiac magnetic resonance feature tracking global and segmental strain in acute and chronic ST-elevation myocardial infarction.

Strain is an important imaging parameter to determine myocardial deformation. This study sought to 1) assess changes in left ventricular strain and ejection fraction (LVEF) from acute to chronic ST-elevation myocardial infarction (STEMI) and 2) analyze strain as a predictor of late gadolinium enhancement (LGE). 32 patients with STEMI and 18 controls prospectively underwent cardiac magnetic resonance imaging. Patients were scanned 8 [Formula: see text] 5 days and six months after infarction (± 1.4 months). Feature tracking was performed and LVEF was calculated. LGE was determined visually and quantitatively on short-axis images and myocardial segments were grouped according to the LGE pattern (negative, non-transmural and transmural). Global strain was impaired in patients compared to controls, but improved within six months after STEMI (longitudinal strain from -14 ± 4 to -16 ± 4%, p < 0.001; radial strain from 38 ± 11 to 42 ± 13%, p = 0.006; circumferential strain from -15 ± 4 to -16 ± 4%, p = 0.023). Patients with microvascular obstruction showed especially attenuated strain results. Regional strain persisted impaired in LGE-positive segments. Circumferential strain could best distinguish between LGE-negative and -positive segments (AUC 0.73- 0.77). Strain improves within six months after STEMI, but remains impaired in LGE-positive segments. Strain may serve as an imaging biomarker to analyze myocardial viability. Especially circumferential strain could predict LGE.

Impact of Sex and Cardiovascular Risk Factors on Myocardial T1, Extracellular Volume Fraction, and T2 at 3 Tesla: Results From the Population-Based, Hamburg City Health Study.

BACKGROUND: Reliable reference intervals are crucial for clinical application of myocardial T1 and T2 mapping cardiovascular magnetic resonance imaging. This study evaluated the impact of sex and cardiovascular risk factors on myocardial T1, extracellular volume fraction (ECV), and T2 at 3T in the population-based HCHS (Hamburg City Health Study). METHODS: The final study sample consisted of 1576 consecutive HCHS participants between 46 and 78 years without prevalent heart disease, including 1020 (67.3%) participants with hypertension and 110 (7.5%) with diabetes. T1 and T2 mapping were performed on a 3T scanner using 5b(3b)3b modified Look-Locker inversion recovery and T2 prepared, fast-low-angle shot sequence, respectively. Stepwise regression analyses were performed to identify variables with an independent impact on T1, ECV, and T2. Reference intervals were defined as the interval between the 2.5% and 97.5% quantiles. RESULTS: Sex was the major independent influencing factor of myocardial native T1, ECV, and T2. Female patients had significantly higher upper limits of reference intervals for native T1 (1112-1261 versus 1079-1241 ms), ECV (23%-33% versus 22%-32%), and T2 (36-46 versus 35-45 ms) compared with male patients (all P<0.001). Cardiovascular risk factors, such as diabetes and hypertension, did not systematically affect native T1. There was an independent association of T2 by hypertension and, to a lesser degree, by left ventricular mass, heart rate (all P<0.001), and body mass index (P=0.001). CONCLUSIONS: Sex needs to be considered as the major, independent influencing factor for clinical application of myocardial T1, ECV, and T2 measurements. Consequently, sex-specific reference intervals should be used in clinical routine. Our findings suggest that there is no need for specific reference intervals for myocardial T1 and ECV measurements in individuals with cardiovascular risk factors. However, hypertension should be considered as an additional factor for clinical application of T2 measurements. REGISTRATION: URL: https://www. CLINICALTRIALS: gov; Unique identifier: NCT03934957.

Myocardial injury detected by T1 and T2 mapping on CMR predicts subsequent cancer therapy-related cardiac dysfunction in patients with breast cancer treated by epirubicin-based chemotherapy or left-sided RT.

OBJECTIVES: Cancer therapy-related cardiac dysfunction (CTRCD) is a relevant clinical problem and needs early prediction. This study aimed to analyze myocardial injury using serial laboratory and cardiac magnetic resonance imaging (CMR) parameters after epirubicin-based chemotherapy compared with left-sided radiotherapy and to study their value for early prediction of CTRCD. METHODS: Sixty-six consecutive women (53 ± 13 years) including n = 39 with epirubicin-based chemotherapy and n = 27 with left-sided radiotherapy were prospectively studied by 3 T CMR including left ventricular (LV) mass and volumes for ejection fraction (LVEF), as well as feature-tracking with global longitudinal strain (GLS) and T1/T2 mapping. CMR was performed at baseline, at therapy completion (follow-up 1, FU1), and after 13 ± 2 months (FU2). CTRCD was defined as LVEF decline of at least 10% to < 55% or a > 15% GLS change at FU2. RESULTS: T1 and T2 increased at FU1 after epirubicin-based chemotherapy, but not after left-sided radiotherapy. CTRCD occurred in 20% of patients after epirubicin-based chemotherapy and in 4% after left-sided radiotherapy. T1 at FU1 was the best single parameter to predict CTRCD with an area under the curve (AUC) of 0.712 (CI 0.587-0.816, p = 0.005) with excellent sensitivity (100%, 66-100%), but low specificity (44%, 31-58%). Combined use of increased T1 and LVEF ≤ 60% at FU1 improved AUC to 0.810 (0.695-0.896) resulting in good sensitivity (78%, 44-95%) and specificity (84%, 72-92%). CONCLUSION: Only epirubicin-based chemotherapy, but not left-sided radiotherapy, resulted in increased T1/T2 myocardial relaxation times as a marker of myocardial injury. Combined use of CMR parameters may allow an early prediction of subsequent CTCRD. KEY POINTS: • Myocardial T1 and T2 relaxation times increased at FU1 after epirubicin-based chemotherapy, but not after left-sided radiotherapy. • Cancer therapy-related cardiac dysfunction (CTRCD) occurred in 20% of patients after epirubicin-based chemotherapy and in 4% after left-sided radiotherapy. • Combined use of increased T1 and reduced LVEF had an AUC of 0.810 (0.695-0.896) to predict CTRCD with good sensitivity (78%, 44-95%) and specificity (84%, 72-92%).

Acute impact of an endurance race on biventricular and biatrial myocardial strain in competitive male and female triathletes evaluated by feature-tracking CMR.

OBJECTIVES: Cardiac adaptation in endurance athletes is a well-known phenomenon, but the acute impact of strenuous exercise is rarely reported on. The aim of this study was to analyze the alterations in biventricular and biatrial function in triathletes after an endurance race using novel feature-tracking cardiac magnetic resonance (FT-CMR). METHODS: Fifty consecutive triathletes (45 ± 10 years; 80% men) and twenty-eight controls were prospectively recruited, and underwent 1.5-T CMR. Biventricular and biatrial volumes, left ventricular ejection fraction (LVEF), FT-CMR analysis, and late gadolinium imaging (LGE) were performed. Global systolic longitudinal (GLS), circumferential (GCS), and radial strain (GRS) were assessed. CMR was performed at baseline and following an endurance race. High-sensitive troponin T and NT-proBNP were determined. The time interval between race completion and CMR was 2.3 ± 1.1 h (range 1-5 h). RESULTS: Post-race troponin T (p < 0.0001) and NT-proBNP (p < 0.0001) were elevated. LVEF remained constant (62 ± 6 vs. 63 ± 7%, p = 0.607). Post-race LV GLS decreased by tendency (- 18 ± 2 vs. - 17 ± 2%, p = 0.054), whereas GCS (- 16 ± 4 vs. - 18 ± 4%, p < 0.05) and GRS increased (39 ± 11 vs. 44 ± 11%, p < 0.01). Post-race right ventricular GLS (- 19 ± 3 vs. - 19 ± 3%, p = 0.668) remained constant and GCS increased (- 7 ± 2 vs. - 8 ± 3%, p < 0.001). Post-race left atrial GLS (30 ± 8 vs. 24 ± 6%, p < 0.0001) decreased while right atrial GLS remained constant (25 ± 6 vs. 24 ± 6%, p = 0.519). CONCLUSIONS: The different alterations of post-race biventricular and biatrial strain might constitute an intrinsic compensatory mechanism following an acute bout of endurance exercise. The combined use of strain parameters may allow a better characterization of ventricular and atrial function in endurance athletes. KEY POINTS: • Triathletes demonstrate a decrease of LV global longitudinal strain by tendency and constant RV global longitudinal strain following an endurance race. • Post-race LV and RV global circumferential and radial strains increase, possibly indicating a compensatory mechanism after an acute endurance exercise bout. • Subgroup analyses of male triathletes with focal myocardial fibrosis did not demonstrate alterations in biventricular and biatrial strain after an endurance race.

Cardiovascular magnetic resonance demonstrates structural cardiac changes following transjugular intrahepatic portosystemic shunt.

Transjugular intrahepatic portosystemic shunt (TIPS) reduces portal hypertension in patients with liver cirrhosis. The exact cardiac consequences of subsequent increase of central blood volume are unknown. Cardiovascular magnetic resonance (CMR) imaging is the method of choice for quantifying cardiac volumes and ventricular function. The aim of this study was to investigate effects of TIPS on the heart using CMR, laboratory, and imaging cardiac biomarkers. 34 consecutive patients with liver cirrhosis were evaluated for TIPS. Comprehensive CMR with native T1 mapping, transthoracic echocardiography, and laboratory biomarkers were assessed before and after TIPS insertion. Follow-up (FU) CMR was obtained in 16 patients (47%) 207 (170-245) days after TIPS. From baseline (BL) to FU, a significant increase of all indexed cardiac chamber volumes was observed (all P < 0.05). Left ventricular (LV) end-diastolic mass index increased significantly from 45 (38-51) to 65 (51-73) g/m2 (P = < 0.01). Biventricular systolic function, NT-proBNP, high-sensitive troponin T, and native T1 time did not differ significantly from BL to FU. No patient experienced cardiac decompensation following TIPS. In conclusion, in patients without clinically significant prior heart disease, increased cardiac preload after TIPS resulted in increased volumes of all cardiac chambers and eccentric LV hypertrophy, without leading to cardiac impairment during follow-up in this selected patient population.

CMR feature tracking strain patterns and their association with circulating cardiac biomarkers in patients with hypertrophic cardiomyopathy.

AIMS: CMR feature tracking strain (CMR-FT) provides prognostic information. However, there is a paucity of data in hypertrophic cardiomyopathy (HCM). We sought to analyze global CMR-FT parameters in all four cardiac chambers and to assess associations with NT-proBNP and cardiac troponin T (hsTnT) in patients with HCM. METHODS: This retrospective study included 144 HCM patients and 16 healthy controls with CMR at 1.5 T. Analyses were performed on standard steady-state free precession cine (SSFP) CMR data using a commercially available software. Global left ventricular (LV) strain was assessed as longitudinal (LVLAX-GLS), circumferential (LVLAX-GCS) and radial strain (LVLAX-GRS) on long -axis (LAX) and as LVSAX-GCS and LVSAX-GRS on short- axis (SAX). Right ventricular (RV-GLS), left atrial (LA-GLS) and right atrial (RA-GLS) strain were assessed on LAX. RESULTS: We found LVLAX-GLS [- 18.9 (- 22.0, - 16.0), - 23.5 (- 25.5, - 22.0) %, p = 0.0001), LVSAX-GRS [86.8 (65.9-115.5), 119.6 (91.3-143.7) %, p = 0.001] and LALAX-GLS [LA2CH-GLS 29.2 (19.1-37.7), LA2CH-GLS 38.2 (34.3-47.1) %, p = 0.0036; LA4CH-GLS 22.4 (14.6-30.7) vs. LA4CH-GLS 33.4 (28.4-37.3) %, p = 0.0033] to be impaired in HCM compared to healthy controls despite normal LVEF. Furthermore, LV and LA strain parameters were impaired in HCM with elevated NT-proBNP and/or hsTnT, despite preserved LVEF compared to HCM with normal biomarker levels. There was a moderate correlation of LV and LA CMR-FT with levels of NT-proBNP and hsTnT. CONCLUSION: CMR-FT reveals LV and LA dysfunction in HCM despite normal LVEF. The association between impaired LV strain and elevated NT-proBNP and hsTnT indicates a link between unapparent functional abnormalities and disease severity in HCM. Typical CMR-FT findings in patients with hypertrophic cardiomyopathy.

Prognosis of early pre-discharge and late left ventricular dilatation by cardiac magnetic resonance imaging after acute myocardial infarction.

To study the long-term prognosis of early pre-discharge and late left ventricular (LV) dilatation in patients with first ST-elevation myocardial infarction (STEMI) treated by percutaneous coronary intervention (PCI) and contemporary medical therapy. Long-term follow-up > 15 years was available in 53 consecutive patients (55 ± 13 years) with first STEMI. Late gadolinium enhanced (LGE) cardiac magnetic resonance imaging (CMR) was obtained at baseline 5 ± 3 days and follow-up 8 ± 3 months after STEMI to measure LV function, volumes and infarct size. Early pre-discharge dilatation was defined as increased left ventricular end-diastolic volume index (LVEDVi) at baseline CMR with > 97 ml/m2 for males and > 90 ml/m2 for females. Late dilatation was defined as initially normal LVEDVi, which increased ≥ 20% at follow-up. Early dilatation was present in 7 patients (13%), whereas late dilatation occurred in 11 patients (21%). Patients with early LV dilatation had highest mortality (57%), whereas patients with late dilatation had similar mortality (27%) compared to patients without dilatation (26%). Multivariate Cox analysis showed that age (P < 0.001), ejection fraction at baseline (P < 0.01) and early dilatation (P < 0.01) were independent predictors of death. Early dilatation qualified as an exclusive independent predictor of long-term mortality after adjustment for age and ejection fraction (P < 0.05, hazard ratio: 2.2, 95% confidence interval: 1.2 to 7.9). Early pre-discharge LV dilatation by CMR enabled strong long-term risk stratification after STEMI. The high mortality of early LV dilatation underscores the clinical importance of this post-infarction complication, which occurred despite PCI and contemporary medical therapy.

Impact of chest wall deformity on cardiac function by CMR and feature-tracking strain analysis in paediatric patients with Marfan syndrome.

OBJECTIVES: To evaluate systolic cardiac dysfunction in paediatric MFS patients with chest wall deformity using cardiac magnetic resonance (CMR) imaging and feature-tracking strain analysis. METHODS: Forty paediatric MFS patients (16 ± 3 years, range 8-22 years) and 20 age-matched healthy controls (16 ± 4 years, range 11-24 years) were evaluated retrospectively. Biventricular function and volumes were determined using cine sequences. Feature-tracking CMR was used to assess global systolic longitudinal (GLS), circumferential (GCS) and radial strain (GRS). A dedicated balanced turbo field echo sequence was used to quantify chest wall deformity by measuring the Haller index (HI). RESULTS: LV volumes and ejection fraction (EF) were similar in MFS patients and controls. There was a trend for lower right ventricular (RV) volume (75 ± 17 vs. 81 ± 10 ml/m2, p = 0.08), RV stroke volume (41 ± 12 vs. 50 ± 5 ml/m2, p < 0.001) and RVEF (55 ± 10 vs. 62 ± 6%, p < 0.01) in MFS patients. A subgroup of MFS patients had an increased HI compared to controls (4.6 ± 1.7 vs. 2.6 ± 0.3, p < 0.001). They demonstrated a reduced RVEF compared to MFS patients without chest wall deformity (50 ± 11% vs. 58 ± 8%, p = 0.01) and controls (p < 0.001). LV GLS was attenuated when HI ≥ 3.25 (- 16 ± 2 vs. - 18 ± 3%, p = 0.03), but not GCS and GRS. LV GLS (p < 0.01) and GCS (p < 0.0001) were attenuated in MFS patients compared to controls, but not GRS (p = 0.31). RV GLS was attenuated in MFS patients compared to controls (- 21 ± 3 vs. - 23 ± 3%, p < 0.05). CONCLUSION: Chest wall deformity in paediatric MFS patients is associated with reduced RV volume, ejection fraction and GLS. Feature-tracking CMR also indicates impairment of systolic LV function in paediatric MFS patients. KEY POINTS: • Paediatric Marfan patients demonstrate reduced RV volume and ejection fraction compared to healthy controls. • A concordant attenuation in RV global longitudinal strain was observed in Marfan patients, while the RV global circumferential strain was increased, indicating a possible compensatory mechanism. • Subgroup analyses demonstrated alterations in RV ejection fraction and RV/LV global strain parameters, indicating a possible association of severe chest wall deformity with biventricular dysfunction in paediatric Marfan patients.

Increased myocardial mass and attenuation of myocardial strain in professional male soccer players and competitive male triathletes.

The purpose of this prospective study was to analyze the relationship between ventricular morphology and parameters of cardiac function in two different athletic groups and controls, using feature tracking cardiac magnetic resonance (FT-CMR). Twenty-three professional soccer players (22 ± 4 years), 19 competitive triathletes (28 ± 6 years) and 16 controls (26 ± 3 years) were included in the study. CMR was performed using a 1.5 T scanner. Cardiac chamber volumes, mass and biventricular global myocardial strain were obtained and compared. In comparison to the control subjects, athletes were characterized by a higher cardiac volume (p < 0.0001), higher cardiac mass (p < 0.001), reduced longitudinal strain of the left and right ventricle (p < 0.05 and p < 0.01 respectively) and reduced left ventricular radial strain (p < 0.05). Soccer players revealed higher amounts of left ventricular mass (87 ± 15 vs. 75 ± 13 g/m2, p < 0.05) than triathletes. Moreover, they showed a greater decrease in left and right ventricular longitudinal strain (p < 0.05 and p < 0.05) as well as in radial left ventricular strain (p < 0.05) in comparison to triathletes. An increase in left ventricular mass correlated significantly with a decrease in longitudinal (r = 0.47, p < 0.001) and radial (r = - 0.28, p < 0.05) strain. In athletes, attenuation of strain values is associated with cardiac hypertrophy and differ between soccer players and triathletes. Further studies are needed to investigate whether it is an adaptive or maladaptive change of the heart induced by intense athletic training.

Acute impact of an endurance race on cardiac function and biomarkers of myocardial injury in triathletes with and without myocardial fibrosis.

AIMS: The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis. METHODS AND RESULTS: Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE-). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE- triathletes (192 ± 30 mmHg, P < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms (P = 0.797) and 989 ± 21 ms versus 989 ± 28 ms (P = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE- triathletes (53 ± 6% vs. 59 ± 6%, P < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE - triathletes (121 ± 30 ml/s/m2) compared to LGE + triathletes (161 ± 34 ml/s/m2, P < 0.01). Post-race atrial peak filling rates increased in LGE- triathletes to 163 ± 46 ml/s/m2, P < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m2, P = 0.747). CONCLUSION: Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.