Funding Acknowledgements Type of funding sources: None. Background Left ventricular (LV) diastolic dysfunction (DD) is a hallmark of hypertrophic cardiomyopathy (HCM) and its phenocopies, such as Fabry disease (FD). Together with left atrial (LA) size, LA function is emerging as a sensitive marker of the adaptive changes to backward transmission of LV cardiac filling pressure, thus implementing DD assessment. Additionally, both HCM and FD are characterized by a primitive atrial myopathy, but LA morpho-functional changes in HCM and FD have never been directly compared. More recently, LA strain by Cardiovascular Magnetic Resonance Feature Tracking (CMR-FT) has been demonstrated to be a feasible and reproducible tool to explore LA function. Purpose To compare LA morpho-functional changes in HCM and FD and to explore their correlation with tissue alterations. Methods 15 HCM and 15 sex-, age- and LV mass index-matched FD patients underwent CMR (Magnetom Aera 1.5T, Siemens) and Doppler Echocardiography for LV diastolic function assessment (E/e’ and DD grading from 0 to 3). LA phasic function was evaluated by CMR-FT strain (Qstrain Medis). The software output included passive (εe, conduit function), active (εa, booster pump function) and total strain (εs, reservoir function), along with LA volumes and ejection fraction (EF). Late gadolinium enhancement (LGE) was quantified as a percentage of LV mass using the standard deviations (SDs) method (≥ 5 SDs). Interstitial fibrosis was assessed by extracellular volume (ECV) quantification in remote myocardium. All patients were in sinus rhythm. Results In the HCM group, the proportion of patients with DD grade 2-3 was only slightly higher than in FD (p 0.26). Accordingly, no significant difference was found in E/e’ value (p 0.78). Compared to FD, HCM patients showed more severe LA morpho-functional changes, including larger LA end-systolic volume (ESV) (113 ± 35 vs 84 ± 23 ml), lower LA EF (37 ± 7 vs 44 ± 9 %) and a greater reduction of εs (-20 ± 5 vs -25 ± 6 %) and εa (-10 ± 4 vs -15 ± 4 %) (all p < 0.05). LV size and function and the burden of fibrosis (LGE quantification and ECV) were comparable between the two groups. Interestingly, in HCM population, unlike in FD, LA morpho-functional measurements significantly correlated with tissue characterization parameters (LA ESV with LGE, r 0.56, p 0.03; εs and εa with ECV, r -0.51, p 0.05 and r -0.59, p 0.02, respectively). Conclusions LA morpho-functional alterations are much more severe in HCM compared to FD with similar degree of LV hypertrophy. A more severe atrial myopathy or different mechanisms of atrial damage in the two cardiomyopathies may explain these findings. LA CMR-FT analysis may represent a sensitive tool to discriminate between HCM and FD, although larger studies are needed to confirm this finding and the possible correlation with the occurrence of atrial arrhythmias and thromboembolic risk.
Funding Acknowledgements Type of funding sources: None. Background Trastuzumab (TZ) is a key therapy for HER-2 positive breast cancer that may have different side effects on the cardiovascular system. One of the most concerning complications is cancer therapy-related cardiac dysfunction (CTRCD). In literature there are conflicting data about the efficacy of heart failure drugs like ACE-inhibitors, ARBs and beta-blockers to prevent such an event. Purpose Aim of this study is to describe our experience on cardioprotective drugs in preventing TZ-related CTRCD. Methods 105 consecutive women affected by HER-2 positive breast cancer treated with TZ referring to our echo-lab were enrolled in our single center prospective study. 3 patients were excluded due to an early TZ suspension not related to cardiovascular complications. Thus 102 patients (97,1%) were eligible for analyses. 86 of these (84,3%) were also treated with Anthracyclines. All patients underwent consecutive transthoracic echocardiography (TTE) before starting TZ and then every 3 months up to 12 months. 2D-Speckle tracking analysis was performed at baseline and at each examination using Tomtec software. A complete clinical evaluation was also performed at each follow up. LV systolic dysfunction was defined as an absolute reduction of LVEF >10% from baseline to LVEF < 53% or a relative reduction of GLS >15% from baseline and a reduction of LVEF >10% from baseline. Results Overall, before starting TZ, 12 patients were taking ACE-inhibitors or ARBs (11,8%) and 5 patients beta-blockers (4,9%). CTRCD occurred in 11 patients (10,8%), among these 9 (81,8%) weren’t taking any heart failure drugs and 5 (45,5%) didn’t present any cardiovascular risk factor. We observed no significant association among cardiovascular risk factors. Use of potential cardioprotective drugs before TZ administration seems to reduce the risk of development of myocardial dysfunction (relative risk 1,67; 95% confidence interval [CI], 0,41 to 6,82; P > 0.05). No clear association was found between any cardiovascular risk factors and CTRCD (relative risk 0,81; 95% confidence interval [CI], 0,26 to 2,47; P > 0.05). Conclusions In HER-2 positive breast cancer patients treated with TZ an early treatment with ACE-inhibitors or ARBs and/or beta-blockers is associated to the prevention of CTRCD. CTRCD seems not to be related to the presence of cardiovascular risk factors. Abstract Figure. Baseline patient characteristics
Aims The most frequent cardiovascular effects induced by electrical injury (EI) are arrhythmias, which occur mostly early after the electrical shock. A few cases of delayed malignant arrhythmias have been described, raising doubts about the helpfulness of heart monitoring after an EI. Methods and results A 46-year-old man experienced an out-of-hospital cardiac arrest four hours after receiving an electrical shock with an alternating voltage of 380 volts from high-pressure water jet cleaner. The out-of-hospital ECG displayed ventricular fibrillation, eight DC shocks were delivered, and return of spontaneous circulation was obtained after 15 minutes. ECG on admission showed bradycardia, HR 55 b.p.m., no clear P waves and prominent T waves in the precordial leads (Figure A). No coronary lesions were detected at the urgent PCI. An ABG on admission revealed lactic acidosis (LAC 18 mmol/L), mild hyperkalaemia (5.19 mmol/L) and mild renal dysfunction (serum creatinine 1.71 mg/dL). Toxicology screen was negative. During the hospital stay, the patient developed a voluminous hematoma and swelling on the right arm, site of the EI. In the following days, blood tests revealed an increase in serum creatinine (peak 4.99 mg/dL), creatine kinase (peak 46186 U/L), liver enzymes (AST peak 2859 U/L and ALT peak 1365 U/L), LDH (peak 2718 U/L) and troponin T (peak 2757 ng/L); these alterations were probably linked to rhabdomyolysis provoked by EI and acute kidney injury was secondary to myoglobinuria. The patient received fluid therapy and furosemide bolus injections. On echocardiography a myxomatous mitral valve with prolapse of both leaflets, mitral annular disjunction and severe mitral regurgitation were displayed (Figure B). Left ventricle was severely dilated with ejection fraction 69%. After improvement in renal function, a cardiac MRI was performed, which ruled out myocardial oedema and displayed subendocardial LGE at the base of the posteromedial papillary muscle (Figure C). The Heart Team opted for mitral valve surgery with P2 resection and mitral valve annuloplasty with 36 mm Carpentier-Edwards Physio II Ring. An ICD was not implanted because the electrical shock and the alteration in electrolytes were considered the primary reasons for cardiac arrest. The patient underwent a cycle of rehabilitation after the intervention and now he does not report any relevant symptom. Conclusion Our patient had bileaflet mitral valve prolapse, mitral annular disjunction and myocardial fibrosis of the papillary muscles, all of which are associated with higher risk of sudden cardiac death. This case highlights that patients with an underlying heart condition predisposing to arrhythmias should promptly seek medical care even after a mild EI for appropriate management.
Funding Acknowledgements Type of funding sources: None. Background Increasing evidence suggests that left atrial (LA) deformation is a sensitive marker of diastolic dysfunction in hypertrophic phenotypes. However, there is little data about the impact of hypertension on LA function; furthermore, LA deformation in hypertensive heart disease (HHD) and hypertrophic cardiomyopathy (HCM) has not been compared yet. Purpose The aim of this study is to compare atrial dimensions and function, evaluated by cardiovascular magnetic resonance feature tracking (CMR-FT) in patients with HHD, HCM and healthy subjects (HS). Methods 67 patients (20 HHD, 27 HCM, 20 HS) underwent CMR and were included in the study. Patients were matched for age, sex and BSA; HHD and HCM were also comparable for LV mass index and ejection fraction (EF). CMR-FT atrial strain analysis was performed using Qstrain, Medis software to obtain i) LA conduit function, ii) LA booster pump function), iii) LA reservoir function, iv) LA volumes and EF. Tissue Doppler echocardiography was used to assess diastolic function, including E/e’. LA stiffness was calculated as the ratio between E/e’ and LA reservoir. Both focal and interstitial myocardial fibrosis were assessed with LGE and extracellular volume (ECV) quantification. Results HHD and HCM showed impaired LA reservoir, conduit function and higher LA volumes vs HS (reservoir: 28 ± 11% and 28 ± 13% vs 41 ± 17%; conduit: 13 ± 7% and 13 ± 7% vs 22 ± 11%; LAESV: 76 ± 21 and 87 ± 22 vs 57 ± 19 ml respectively; all p ≤ 0.03). HHD and HCM were comparable for bi-ventricular morpho-functional parameters and ECV. HHD showed lower E/e’ values (8 ± 2 vs 16 ± 7, p = 0.002) and LA stiffness (0.23 ± 0.3 vs 0.74 ± 0.6, p 0.03), LA dimensions (LA area 13 ± 3 vs 16 ± 3 cm2/m2, p = 0.02 , LAESVi 41 ± 12 vs 48 ± 11 ml/m2, p = 0.05) and LGE extent (1 ± 2% vs 5 ± 5%, p = 0.001) as compared to HCM. Interestingly, HHD revealed a comparable reduced LA reservoir and conduit function (all p = 0.9) vs HCM. In HHD patients LA reservoir function was correlated with E/e’ (r -0.8, p = 0.02), but not in HCM. Conversely, LA reservoir function was correlated with LV mass index in HCM (r -0.5, p < 0.01). Conclusions HHD patients showed a similar and significant impairment of LA function, with lower LA dimensions and E/e’ compared to HCM with similar LV mass index and preserved function. CMR-FT atrial strain analysis could represent a useful tool for HHD management, able to detect diastolic dysfunction (and/or atrial dysfunction) earlier than traditional markers. Further studies are needed to explore the relationship of LA deformation to heart failure symptoms and atrial fibrillation occurrence and potential changes related to response to therapy.
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