Predictors of the voltage derived left atrial fibrosis in patients with long-standing persistent atrial fibrillation.

BACKGROUND: Left atrial (LA) arrhythmogenic substrate beyond the pulmonary veins (PV) seems to play a crucial role in the maintenance of atrial fibrillation (AF). The aim of this study was to evaluate the association of selected parameters with the presence and extent of voltage-defined LA fibrosis in patients with long-standing persistent AF (LSPAF) undergoing catheter ablation. METHODS: One hundred and sixteen consecutive patients underwent high density-high resolution voltage mapping of the LA with a multielectrode catheter following PV isolation and restoration of sinus rhythm with cardioversion. A non-invasive dataset, such as clinical variables, two-and three-dimensional echocardiography determined LA size and function and fibrillatory-wave amplitude on a standard surface electrocardiogram were obtained during AF before ablation. RESULTS: Low-voltage areas (LVA; 15 cm² [IQR 8-31]) were detected in 56% of patients. Twenty nine percent of them presented mild, 43% moderate and 28% severe global LVA burden. In univariate analysis, age ≥ 57 years old, female sex, body surface area ≤ 1.76 m², valvular heart disease, moderate mitral regurgitation, chronic coronary syndrome, hypothyroidism, CHA2DS2-VASc score ≥ 3 and ≥ 4 predicted the presence of LVA. In multivariate analysis only female sex, valvular heart disease and CHA2DS2-VASc ≥ 4 remained statistically significant. AF duration, LA size and function and fibrillatory-waves amplitude were neither associated with the prediction of the LVA, nor severe LVA burden. CONCLUSIONS: A LSPAF diagnosis does not indicate the presence of voltage defined fibrosis in many cases. Simple non-invasive screening of the LSPAF population could predict LVA prevalence.

Association of Adiponectin, Leptin and Resistin Plasma Concentrations with Echocardiographic Parameters in Patients with Coronary Artery Disease.

The imbalanced network of adipokines may contribute to the development of systemic low-grade inflammation, metabolic diseases and coronary artery disease (CAD). In the last decade, three classic adipokines-adiponectin, leptin and resistin-have been of particular interest in studies of patients with CAD due to their numerous properties in relation to the cardiovascular system. This has directed our attention to the association of adipokines with cardiac structure and function and the development of heart failure (HF), a common end effect of CAD. Thus, the purpose of this study was to analyse the associations of plasma concentrations of adiponectin, leptin and resistin with parameters assessed in the echocardiographic examinations of CAD patients. The presented study enrolled 167 Caucasian patients (133 male; 34 female) with CAD. Anthropometric, echocardiographic and basic biochemical measurements, together with plasma concentrations of adiponectin, leptin and resistin assays, were performed in each patient. Adiponectin concentrations were negatively associated with left ventricular ejection fraction (LVEF) and shortening fraction (LVSF), and positively associated with mitral valve E/A ratio (E/A), left ventricular end-diastolic volume (LVEDV), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter LVESD, and left atrium diameter (LAD). Resistin concentrations were negatively associated with E/A. Leptin concentrations, although correlated with HF severity assessed by the New York Heart Association (NYHA) Functional Classification, were not independently associated with the echocardiographic parameters of cardiac structure or function. In conclusion, adiponectin and resistin, but not leptin, are associated with the echocardiographic parameters of cardiac remodelling and dysfunction. These associations suggest that adiponectin and resistin might be involved in mechanisms of cardiac remodelling or compensative response. We also suggest the possible benefits of adiponectin and resistin level measurements in the monitoring of patients with CAD.

Atrial fibrillation risk scores to evaluate left atrial substrate based on voltage analysis in long-standing persistent type of arrhythmia.

BACKGROUND: Pre-ablation identification of left atrial (LA) low voltage areas (LVA) among long-standing persistent atrial fibrillation (LSPAF) population remains challenging. AIMS: The aim of the study was to analyze the potential of selected scores originally developed to assess arrhythmia recurrences, thromboembolic complications, or progression from paroxysmal to persistent AF to predict the presence of LA-LVA in LSPAF patients. METHODS: One hundred and fifty-two patients underwent pulmonary vein isolation followed by high-density-high-resolution LA voltage mapping. AF risk scores, such as APPLE, ATLAS, CAAP-AF, DR-FLASH, CHA2DS2-VASc, and HATCH were retrospectively calculated. A receiver operating characteristic curve analysis was performed to evaluate the ability of the scores to predict LVA. RESULTS: Low voltage areas were detected in 52% of the patients. 28% of the patients with LVA presented severe global LVA burden, whereas 56% of the patients showed a disseminated pattern of remodeling. CAAP-AF ≥7, DR-FLASH ≥4, and CHA2DS2-VASc ≥3 predicted the presence of LVA, whereas ATLAS ≤7 indicated the absence of LVA. ATLAS ≤8, CAAP-AF ≤9, DR-FLASH ≤4, and CHA2DS2-VASc ≤3 predicted the absence of severe LVA. APPLE ≤3 and CHA2DS2-VASc ≤2 predicted the absence of a LVA disseminated pattern. Among predictive scores, ATLAS (AUC, 0.633, 95% CI, 0.543-0.723, P = 0.004), DR-FLASH (AUC, 0.696; 95% CI, 0.594-0.81; P <0.001), and CHA2DS2-VASc (AUC, 0.644; 95% CI 0.518-0.77; P = 0.025) were the best predictors for the absence of LVA, severe LVA and a disseminated pattern of LVA, respectively. CONCLUSIONS: Atrial fibrillation risk stratification with specific scoring systems can unmask the presence of LA-LVA in the LSPAF population.

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation.

It was hypothesised that left atrial (LA) fibrosis identified by the presence of low-voltage areas (LVA) may influence the mechanical and electrical function of the left (LAA) and right (RAA) atrial appendage among the long-standing persistent atrial fibrillation (LSPAF) population. 140 consecutive patients underwent voltage mapping of LA with a multielectrode catheter following pulmonary vein isolation and restoration of sinus rhythm with cardioversion. Echocardiography determined LAA peak outflow and inflow velocities and intracardiac catheter-based mean LAA and RAA AF cycle length (AFCL) were obtained during AF before ablation. The impact of flow velocities and AFCL on the prevalence and location of LVA was further evaluated. LVA were detected in 54% of the patients. 14% of the patients presented severe global LVA burden > 20% of the total LA surface area. 29% of the patients presented a disseminated pattern of remodelling as 3 out of 5 LA segments were affected. LAA AFCL, RAA AFCL, LAA flow velocities did not predict the absolute presence of LVA. However LAA AFCL > 155 ms predicted disseminated LVA pattern and LAA AFCL > 165 ms severe LVA incidence. LAA AFCL > 155 ms was predictive for existence of LVA within antero-septal LA segments whilst LAA emptying velocity ≤ 0.2 m/s within lateral wall. Moreover RAA AFCL > 165 ms was strongly related to the presence of LAA AFCL > 15 ms and > 165 ms. LAA and RAA functional assessment was predictive of the presence of advanced stages of voltage-defined LA fibrosis and its regional distribution among LSPAF population.

The paradox of the first cycle of chemotherapy-transient improvement of contractility and diastolic function after the first cycle of anthracycline-based chemotherapy: a prospective clinical trial.

AIMS: Breast cancer is the most common cancer among women, and anthracyclines are the most commonly administered drugs for these patients. Cardiotoxicity is one of the complications, which limits the success of this therapy. Very few studies have evaluated anthracycline toxicities within the first few hours after the first infusion, and the majority of published studies were performed in animal models. The present study aimed to evaluate changes in echocardiographic parameters in women with breast cancer 24 hours after receiving the first dose of an anthracycline. MATERIALS AND METHODS AND RESULTS: The present study included 75 chemotherapy-naive female patients without heart failure, who were diagnosed with breast cancer and were scheduled to undergo anthracycline-based chemotherapy (epirubicin and doxorubicin). During their visits to the Heart Center, the patients underwent detail echocardiographic examination, including assessment of systolic and diastolic function and longitudinal strain. There were no differences in baseline echocardiographic parameters between patients with and those without cardiotoxicity. Cardiotoxicity was observed during follow-up in 14 patients (18.7%). Improvements in left ventricular ejection fraction and global longitudinal strain were observed at 24 hours after administration of the cytotoxic agent in the subgroup of patients without further cardiotoxicity. The changes were transient and the assessment of left ventricular ejection fraction after completion of chemotherapy revealed similar values to those before the treatment. CONCLUSIONS: The findings of our study suggest that transient improvement in contractility and systolic and diastolic function might occur 24 hours after anthracycline administration, especially in patients who do not develop cardiotoxicity.

Chemotherapy and echocardiographic indices in patients with non-Hodgkin lymphoma: the ONCO-ECHO study.

The cardiotoxicity of chemotherapy (CTx) for non-Hodgkin's lymphomas is not well recognized. In order to facilitate individual risk counseling for patients, we analyzed the effect of CTx on echocardiographic indices in regard to clinical data in patients treated for non-Hodgkin's lymphoma (NHL). A prospective multicenter ONCO-ECHO trial included 67 patients with NHL (45 patients with DLBCL (diffuse large B cell lymphoma) and 22 with non-DLBCL). Patients received standard CTx, primarily R-CHOP, CHOP, R-COP and COP regimens. Clinical data and echocardiographic indices were obtained at baseline, 3-, 6- and 12-month follow-up. The primary end point representing CTx cardiotoxicity was defined as a ≥ 10% decrease in the left ventricular ejection fraction (LVEF) during 12-month observation. In a 12-month follow-up five (7.5%) deaths occurred, while no clinical manifestations of heart failure were reported. There was an increase in left ventricular end-systolic diameter (p = 0.002) and E/e' index (p = 0.036) in 12-month observation. Preexisting coronary artery disease was associated with significant decrease in the ΔLVEF (p = 0.008), increase in ΔLVEDV (p = 0.03) and ΔLVESV (p = 0.02) and increase in the Δ left atrium diameter (p = 0.02); while history of arterial hypertension was related to significant decrease in the ΔLVEF (p = 0.039), diabetes mellitus was related to significant increase in the ΔE/e' index (p = 0.002). The primary end point was reported in ten (14.9%) patients. There were no independent risk factors for cardiotoxicity in the study population. Chemotherapy administered to NHL patients may induce dilatation and impaired LV diastolic function. Standard cardiovascular risk factors may predispose patients to negative LV remodeling.

Scuba diving, patent foramen ovale and heart rhythm disturbances: The role of underwater Holter monitoring-Case report.

Patent foramen ovale (PFO) is thought to be a risk factor for decompression illness (DCI). Catheter-based closure procedure reduces the risk of DCI in selected scuba divers with PFO. Major complication of invasive approach are rare, minor, especially heart rhythm disturbances are reported relatively often. We describe a case of 41-year-old diver, who underwent PFO closure due to recurrent DCI events. Afterward, he experienced no DCI symptoms; however, he complained about feeling of the heart beating during a submersion. Arrhythmia should be considered as a life-threatening for scuba diver, thus we performed underwater ECG monitoring and exclude the arrhythmia.

Tissue Doppler echocardiography detects subclinical left ventricular dysfunction in patients undergoing chemotherapy for colon cancer: insights from ONCOECHO multicentre study.

BACKGROUND: Colorectal cancer (CRC) is the second most common cancer in women and the third in men in Poland. The role of chemotherapy (CTX) depends on the stage of CRC: adjuvant CTX is a standard treatment in stage III and should also be considered in stage II with risk factors. AIM: The aim of the paper was to assess the cardiovascular consequences of CTX in CRC enrolled to the ONCOECHO multicentre study (2012-2014). To identify potential cardiotoxicity, we focused on myocardial function, heart rhythm and conduction disorders, and adverse cardiovascular events. METHODS: Twenty-five CRC patients (12 women, mean age 61.3 [35-76] years), all receiving six-month adjuvant CTX were included. Thirteen patients received 5-fluorouracil (5FU)-based CTX, and 12 patients received a capecitabine-based scheme. Subjects were assessed at baseline and followed-up three, six, and 12 months after the onset of treatment. In this analysis we focused on conduction abnormalities, systolic and diastolic function of the left ventricle (LV), and cardiovascular events. RESULTS: In 12-month follow-up a decrease of selected tissue Doppler parameters (e.g. S'IVS, S'lat, and E'sept) was observed, and it was significant. LV structural parameters and ejection fraction (EF) remained unaffected. Changes in myocardial performance were not influenced by CTX regimen or treatment with beta-blockers or angiotensin-converting enzyme inhibitors. CTX did not affect LV structural parameters, EF, or conduction system, nor was it associated with cardiovascular events during the 12-month follow-up. CONCLUSIONS: CTX in CRC patients does not affect LV structural parameters and EF. It may, however, trigger subtle changes in myocardial performance detectable by tissue Doppler echocardiography after 12 months. Moreover, it causes a transient increase of QT, which resolves after CTX cessation.

Alcohol septal ablation in hypertrophic cardiomyopathy utilizing a longitudinal 17-year study (mean 10.8). Observation follow-ups taken at a single medical centre.

BACKGROUND: Alcohol septal ablation (ASA) is a method of treatment in obstructive hypertrophic car-diomyopathy (HOCM), but there is little data on the long-term results of ASA and the natural course after treatment. The aim of the study was to evaluate the results of ASA in HOCM in multiannual observation, and its impact on patient survival, exercise capacity, electrical complications, and changes in the anatomy and function of the heart. METHODS: The study evaluated 47 patients with HOCM with a high left ventricular outflow tract (LVOT gradient) treated between 1997 and 2014 with ASA. Annual examinations evaluated the clinical condi-tion, at rest and with exercise electrocardiogram, Holter monitoring, echocardiography, the evolution of HOCM towards the dilated form, and the frequency of pacemaker implantation. RESULTS: The analysis included data from 34 patients under observation for 3 to 17 (mean 10.8) years. Their age at procedure was 21-65, a mean of 47 years. All patients had permanently reduced LVOT gradient with a mean of 77.36 ± 35.46 to 11.40 ± 10.85 and showed improvement in the performance I to II New York Heart Association. Two out of five deaths had possible cardiac etiology. Fifteen patients received a pacemaker or cardioverter implants. In 4 subjects the long-term observation revealed new wall contractility abnormalities, interpreted as a shift of HOCM to the dilated form. CONCLUSIONS: Alcohol septal ablation permanently eliminated the gradient in LVOT and improved the performance of patients, however it did not prevent a shift of HOCM to the dilated form. Pacemaker implantations are relatively frequent. (Cardiol J 2017; 24, 2: 125-130).

Inflammation markers are associated with metabolic syndrome and ventricular arrhythmia in patients with coronary artery disease.

BACKGROUND: Inflammation plays a major role in the development and progression of atherosclerosis and coronary artery disease (CAD). Inflammation markers, including white blood cell (WBC) count, C-reactive protein (CRP) and interleukin-6 (IL-6), are widely used for cardiovascular risk prediction. The aim of the study was to establish factors associated with WBC, CRP and IL-6 in patients with CAD. Two functional polymorphisms in genes encoding enzymes participating in adenosine metabolism were analyzed (C34T AMPD1, G22A ADA). METHODS: Plasma concentrations of IL-6 were measured using high-sensitivity ELISA kits, and the nephelometric method was used for high-sensitivity CRP (hs-CRP) measurement in 167 CAD patients. RESULTS: Presence of metabolic syndrome (MS) and its components, presence of heart failure, severity of CAD symptoms, severe past ventricular arrhythmia (sustained ventricular tachycardia [sVT] or ventricular fibrillation [VF]), lower left ventricle ejection fraction, higher left ventricle mass index, higher end-diastolic volume and higher number of smoking pack-years were significantly associated with higher WBC, CRP and IL-6. Strong associations with arrhythmia were observed for IL-6 (median 3.90 vs 1.89 pg/mL, p<0.00001) and CRP concentration (6.32 vs 1.47 mg/L, p=0.00009), while MS was associated most strongly with IL-6. CRP and IL-6 were independent markers discriminating patients with sVT or VF. There were no associations between AMPD1 or ADA genotypes and inflammation markers. CONCLUSIONS: WBC, CRP and IL-6 are strongly associated with components of the metabolic syndrome. Their strong association with life-threatening ventricular arrhythmia emphasizes the proarrhythmic role of inflammation in the increased cardiovascular risk of CAD patients.

[The role of biochemical markers with special regard to troponin, CK-MB, NT-proBNP as early biomarkers of cardiotoxicity among women after chemotherapy due to breast cancer].

Introduction: Cardiotoxicity of drugs in oncology is a growing problem which cardiologists and oncologists have to struggle with. So far, researchers have been looking for biochemical markers which could help to extract a group more prone to developing complications after chemotherapy. Authors' reports are inconsistent in this topic. Aim: This study assesses the role of troponin I, CK-MB and NT-proBNP as early predictive markers for later cardiotoxicity among patients with breast cancer treated with chemotherapy. Methods: One hundred five patients with breast cancer, without either heart failure or more than moderate severity of valvular heart diseases were qualified to the study. Results: NT-proBNP concentration significantly increased just after the first cycle of chemotherapy, either in a subgroup which developed cardiotoxicity or without this end point (p<0.001, p=0.004). CK-MB did not change significantly during observation. Troponin I did not change in any of the patients. During observation HDL-cholesterol concentration significantly decreased. A transient increase of the concentration of LDL-cholesterol had been noted, but later it decreased below baseline level. Conclusion: Troponin I has too low sensitivity to be used as a prognostic marker for further cardiotoxicity after chemotherapy. No prognostic values have been noted of NT-proBNP and CK-MB due to the lack of differences in both a subgroup with and without cardiotoxicity.

Effect of cardiac resynchronisation therapy on coronary blood flow in patients with non-ischaemic dilated cardiomyopathy.

BACKGROUND: Cardiac resynchronisation therapy (CRT) has beneficial effects on cardiac function, exercise tolerance, symptoms, and prognosis. Coronary blood flow impairment has been observed in patients with non-ischaemic dilated cardiomyopathy (DCM) despite angiographically normal coronary arteries. No data are available on coronary blood flow and coronary flow reserve (CFR) measured by intracoronary Doppler in different coronary arteries in patients with DCM and left bundle branch block (LBBB) before and during treatment with CRT. AIM: Thus, the major aim of our study was to assess the effect of CRT on coronary blood flow in patients with non-ischaemic DCM and to compare coronary blood flow and CFR measured in the 3 major coronary arteries (left anterior descending [LAD], left circumflex [LCX], and right coronary artery [RCA]). METHODS: Twenty one patients with DCM and LBBB (mean left ventricular ejection fraction 26 ± 7%, 5 females, mean age 57.8 ± 8.1 years) were studied. Average peak velocity, diastolic/systolic velocity ratio and CFR were measured using intracoronary Doppler before and 6-9 months after implantation of CRT-D or CRT-P. RESULTS: In patients with a clinical improvement (71.4%), CFR increased in LAD. CFR measured in LCX and RCA did not improve either in the overall study group or in patients with a clinical improvement. The observed increase in CFR in LAD correlated only with reduction of QRS duration. CONCLUSIONS: In non-ischaemic DCM, CFR is reduced only in LAD. A significant improvement of CFR in LAD after CRT correlates with reduction of QRS duration.

Tako-tsubo cardiomyopathy following complete atrioventricular nodal heart block during transcatheter radiofrequency ablation of atrioventricular nodal reentrant tachycardia.

We report a case of tako-tsubo cardiomyopathy after an unintentional atrioventricular (AV) block during an ablation procedure in a 77 year-old woman. This intriguing case explores three possible reasons that could have triggered the disease: (1) slow pathway destruction; (2) AV nodal complete heart block; (3) the overall stress the patient had experienced.

Sudden death in hypertrophic cardiomyopathy: old risk factors re-assessed in a new model of maximalized follow-up.

AIMS: in hypertrophic cardiomyopathy (HCM), the following five risk factors have a major role in the primary prevention of sudden death (SD): family history of SD (FHSD), syncope, massive wall thickness (MWTh) >30 mm, non-sustained ventricular tachycardia (nsVT) in Holter monitoring of electrocardiography, and abnormal blood pressure response to exercise (aBPRE). In HCM, as a genetic cardiac disease, the risk for SD may also exist from birth. The aim of the study was to compare the survival curves constructed for each of the five risk factors in a traditional follow-up model (started at the first presentation of a patient at the institution) and in a novel follow-up model (started at the date of birth). In an additional analysis, we compared the survival rate in three subgroups (without FHSD, with one SD, and with two or more SDs in a family). METHODS AND RESULTS: a total of 1306 consecutive HCM patients (705 males, 601 females, mean age of 47 years, and 193 patients were <18 years) evaluated at 15 referral centres in Poland were enrolled in the study. In a novel method of follow-up, all the five risk factors confirmed its prognostic power (FHSD: P = 0.0007; nsVT: P < 0.0001; aBPRE: P = 0.0081; syncope: P < 0.0001; MWTh P> 0.0001), whereas in a traditional method, only four factors predicted SD (except aBPRE). In a novel model of follow-up, FHSD in a single episode starts to influence the prognosis with a delay to the fifth decade of life (P = 0.0007). Multiple FHSD appears to be a very powerful risk factor (P < 0.0001), predicting frequent SDs in childhood and adolescence. CONCLUSION: the proposed concept of a lifelong calculated follow-up is a useful strategy in the risk stratification of SD. Multiple FHSD is a very ominous risk factor with strong impact, predicting frequent SD episodes in the early period of life.

Association of C34T AMPD1 gene polymorphism with features of metabolic syndrome in patients with coronary artery disease or heart failure.

OBJECTIVE: The common C34T polymorphism in the AMP deaminase-1 (AMPD1) gene results in an inactive enzyme in homozygotes for the mutated T allele. Some studies have shown an association of T allele with longer survival in heart failure (HF) and/or coronary artery disease (CAD). The aim of this study was to assess genotype-phenotype correlations in such patients, with emphasis on components of the metabolic syndrome. METHODS: Ninety-seven patients with CAD without HF (CAD+ HF-) and 104 with HF (HF+) were genotyped by PCR-RFLP. The genetic control group comprised 200 newborns. RESULTS: No significant differences were found in the frequency of AMPD1 genotypes between the groups. In the CAD+ HF- group, the carriers of T allele compared to CC homozygotes had significantly lower values of waist circumference (89.5+/-8.5 versus 97.7+/-11.2 cm; p = 0.00029), waist/hip ratio (p = 0.0059) and BMI (p = 0.045). There was no diabetes or fasting glycaemia > or =126 mg/dL in T carriers, while these features were present in 25% of CC homozygotes (p = 0.0024). In the HF+ group, a tendency towards a lower prevalence of diabetes (20 % versus 41%; p = 0.068) and significantly lower systolic blood pressure (p = 0.048) were observed in T allele carriers. CONCLUSIONS: C34T AMPD1 polymorphism may be associated with reduced frequency of obesity in CAD patients and of hyperglycaemia and diabetes in both CAD and HF patients. Morphometric parameters associated with adipose tissue distribution and parameters of glucose metabolism should be analysed as potential confounders in further studies on the role of polymorphisms of AMPD1 and other genes associated with AMP and adenosine metabolism in cardiovascular disease.