Cause Of Left Ventricular Dysfunction Research Articles

Clinical impact of multimodality assessment of myocardial viability

AbstractCoronary artery disease (CAD) is a prevalent cause of left ventricular dysfunction. Nevertheless, effective elective revascularization, particularly surgical revascularization, can enhance long‐term outcomes and, in selected cases, global left ventricular contractility. The assessment of myocardial viability and scars is still relevant in guiding treatment decisions and selecting patients who are likely to benefit most from blood flow restoration. Although the most recent randomized studies challenge the notion of “hibernating myocardium” and the clinical usefulness of assessing myocardial viability, the advancement of imaging techniques still renders this assessment valuable in specific situations. According to the guidelines of the European Society of Cardiology, non‐invasive stress imaging may be employed to define myocardial ischemia and viability in patients with CAD and heart failure before revascularization. Currently, several non‐invasive imaging techniques are available to evaluate the presence and extent of viable myocardium. The selection of the most suitable technique should be based on the patient, clinical context, and resource availability. This narrative review evaluates the characteristics of available imaging modalities for assessing myocardial viability to determine the most appropriate therapeutic strategy.

Left bundle branch block cardiomyopathy: an intriguing and defiant entity from diagnosis to treatment

Abstract Introduction and objectives Left bundle branch block cardiomyopathy (LBBB-CM) is an increasingly recognized entity, where electromechanical dyssynchrony seems to play a central role in left ventricular dysfunction (LVD) development. This is a challenging and scarcely studied topic, as causality dilemma between LBBB and LVD is still unsolved. Our aim is to increase current evidence on the subject by analyzing a population of idiopathic LBBB patients (pts) who developed, at some point, LVD not explained by other causes. Methods Retrospective study of LBBB adult pts screened from a large tertiary care hospital electrocardiographic database from 2011 to 2017. After careful evaluation, only possible LBBB-CM pts with serial follow-up (FU) echocardiographic and clinical data were included in the analysis. Results 53 pts were identified as possible LBBB-CMP. At baseline, 44% presented left ventricular ejection fraction (LVEF)>50%, while 56% had LVD. 51% were female and mean age at first-ever LBBB report was 59 years-old. All cohort presented echocardiographic mechanical desynchrony, and additional testing to exclude other causes of LVD (non-invasive ischemia testing in 78%; coronariography in 68%; cardiac magnetic resonance in 38%). Median FU time was 10 years. Worst-LVD was reported as severe in 49% of pts, moderate in 23% and mild in 28%. Median time-to-dysfunction in those with initial LVEF>50% was 8 years. 77% of pts presented heart-failure (HF) symptoms. 40% and 42% presented at least 1 CV event and CV hospitalization, respectively. Most events and/or hospitalizations were due to acute decompensated HF. 2 CV deaths were observed. Cardiac resynchronization therapy (CRT) devices were implanted in 47% of pts. All presented clinical improvement after implantation, and LVEF significantly increased (pre-CRT median LVEF of 24% vs 48% post-CRT; p<0.001). When comparing pts with vs without CRT (Figure 1), better LVEF improvements were achieved in CRT group (median LVEF improvement of 27% in CRT vs 11%; p<0.001). Repeating the latter analysis in pts who only presented at least moderate dysfunction, higher LVEF increase was also reported in CRT group (median LVEF improvement of 27% in CRT pts vs 14%; p=0.002), and significantly more CRT pts recovered LV function (50% CRT vs 14% non-CRT; p=0.028). Notably, no differences were found in rates of medical HF therapy between groups (p=1). Conclusion Our data shows LBBB-CM as a diagnosis of exclusion, where careful evaluation of other LVD etiologies should be performed and discarded. We highlight important morbidity rates in this population, namely HF hospitalizations, as well as the apparently critical role of CRT implantation in these pts. All our CRT pts responded excellently to the therapy. Thus, our study raises awareness to the emerging question of whether this entity can be reversed after LBBB correction with CRT and if early intervention would be desirable.Figure 1

A potential cause of left ventricular dysfunction after surgery in neonates with low-risk congenital diaphragmatic hernia: high-tension repair.

Congenital diaphragmatic hernia (CDH) is a serious congenital malformation. Given the focus on improving survival in patients with "high-risk" CDH, it is possible that risk factors for low-risk patient with CDH may not be a concern. Left heart failure leads to adverse postoperative outcomes, including the need for extracorporeal membrane oxygenation (ECMO). The purpose of this study was to explore the causes of postoperative left heart failure in the low-risk group. A retrospective study was conducted on newborns with congenital diaphragmatic hernia who were surgically treated in our hospital from January 2018 to March 2022. Children at low risk were divided into three groups according to the intraoperative repair conditions. Group A was defined as grade A defects repaired by direct suture. Group B was defined as a grade B defect repaired by mesh. Group C was a grade B defect repaired by high-tension suture. The age, gender, weight, perioperative echocardiography, and follow-up of the patients were statistically analyzed. The risk factors of left ventricular dysfunction after surgery in neonates with low-risk congenital diaphragmatic hernia were analyzed. A total of 52 low-risk children were included in the study. For children in the low-risk group, there was no significant difference between the low-tension repair group and the high-tension repair group in terms of operation time, thoracic tube drainage time, hospital stay, and long-term survival rate. Group A and group B showed good left ventricular function, while group C showed more decreased left ventricular EF and LVFS (LVEF 54.06 ± 10.28, LVFS 26.94 ± 5.83, p < 0.001). On the comparison of measures of left ventricular size, the mean values of left ventricular end-diastolic diameters(LVDD) and left ventricular end-systolic diameters (LVDS) were significantly difference in group C. Univariate analysis showed that LHR, o/e LHR, operation time, and high-tension repair were the influencing factors of left ventricular dysfunction. Multivariate logistic regression analysis identified risk factors for high-tension repair. Severe left heart dysfunction occurred in 2 patients with ECMO requirement in the high-tension repair group, although the difference was not significant. High-tension repair is a potential cause of left ventricular dysfunction in neonates with low-risk CDH.

Correlation of left ventricular mechanical dyssynchrony in patients with chronic kidney disease using phase analysis of gated single photon emission computed tomography myocardial perfusion imaging

Abstract Background Left ventricular mechanical dyssynchrony (LVMD) possesses deleterious effects that have been neglected in chronic kidney disease (CKD) as a cause of left ventricular dysfunction and further progression to heart failure, possibly contributing to sudden cardiac death in this population. Thus, cardiovascular risk assessment is essential in early stages of CKD as well as in the pre-transplant screening and this can be performed non-invasively by modalities including phase analysis Gated-SPECT myocardial perfusion imaging (MPI). This modality has emerged as a prognostic tool to predict mortality independent of MPI abnormalities as well as assessment of ventricular synchrony. Purpose The goal of this study is to evaluate the relationship of left ventricular mechanical dyssynchrony using phase analysis G-SPECT and chronic kidney disease severity and its predictors. Methods We included 567 patients who underwent one day rest/stress (dipyridamole) 99mTc-sestamibi myocardial perfusion imaging with G-SPECT for the following indications for testing: detection of CAD among asymptomatic patients, risk assessment during pre-operative evaluation for kidney transplantation and evaluation for noncardiac surgery without active cardiac conditions between January 2017 to January 2021. Data was collected including gender, age, risk factors resting heart rate and baseline blood pressure. Gated SPECT-MPI was performed according to the protocol rest followed by stress images (dipyridamole) 99mTc-sestamibi. The rest and stress phase analysis (histogram bandwidth, standard deviation of phase and entropy) parameters were compared between the five stages of chronic kidney disease. Data of the stress-rest difference in dyssynchrony was analyzed using McNemar's test; crude odds ratios and adjusted odds or multivariate analysis were done. Results Advanced CKD (Stage 4–5) shows statistically significant correlation with the Histogram bandwidth (HBW) both at stress (p=0.008) and rest (p=0.018), and stress entropy (p=0.007). As for the other stages, LVMD is present with similar results seen with the phase parameters HBW and PSD, the entropy values at rest than at stress for Stages I to IV (p&amp;lt;0.05). On further analysis, abnormal perfusion showed to be an independent predictor of left ventricular mechanical dyssynchrony across all arms. Other associated factors includes advanced CKD (stages 4–5), male sex, BMI ≥30 kg/m2, blood pressure and resting heart rate were significantly associated with increased odds of dyssynchrony across stress and rest tests. Overall, the full models were statistically significant, with R-squared ranging from 14.96% to 30.11% (p&amp;lt;0.001). Conclusion This study showed that CKD patients have left ventricular mechanical dyssynchrony on gated-SPECT MPI. Hence, it can be used as an alternative for early assessment and guide decision making for the treatment of patients with CKD to prevent further cardiovascular complication. Funding Acknowledgement Type of funding sources: None.

Acute cardiac injury (ACI) in COVID-19 pneumonia

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Since the SARS-CoV2 break-out many reports focused on the role of cardiovascular system involvement in the patient’s outcome(1). However, few descriptions exist including only patients with severe ARDS admitted to general ICU. Methods We enrolled adult patients with severe ARDS related to COVID-19 infection consecutively admitted to ICU between February 2020 and March 2021. Acute cardiac injury was defined as a rise and fall of cTnI above the 99th percentile (i.e., ≥ 47 ng/L)(2). Hs-TnI was measured at admission and during ICU stay. Echocardiographic examinations were performed at ICU admission and at the time of worst cTnI. Left ventricular (LV) and right ventricular (RV) systolic dysfunction were defined respectively as LV ejection fraction (LVEF) &amp;lt; 50% and as tricuspid annular plane systolic excursion (TAPSE) &amp;lt; 16 mm. Results A total of 148 patients were included in the analysis. Acute cardiac injury was present in 65 (44.9%) cases at admission. Forty-seven (21.8%) patients had isolated depressed LVEF, 13 (9.0%) had isolated RV systolic dysfunction and 24 (16,4%) presented with biventricular systolic dysfunction. Eithy-two (56.1%) had a worsening of hs-TNI values during the admission of whom a consensual worsening of LVEF and TAPSE was observed in respectively 32 (21.8%) and 28 (19.2%) patients. Cardiac injury at ICU admission yielded an increased risk of in-hospital mortality (OR 1.30 [95% CI 0.71 – 2.38]) (Figure 1 – left panel) as well as the presence of impaired echocardiography (OR 1.85 [95% CI 1.01 – 3.40]) (Figure 1 – right panel). Worst hs-TNI correlated with worst procalcitonin (PCT) values (p &amp;lt;0.001 r20.81) in case of on-going septic shock and 85 % of patients with RV dysfunction had either evidence of pulmonary thrombus at CT scan or high inspiratory peak pressure (&amp;gt; 30 cmH2O) at mechanical ventilation (respectively, p &amp;lt; 0.001 and p &amp;lt;0.01). Bivariable analysis adjusted for the inverse probability of having an impaired echocardiographic exam confirmed the increased risk of in-hospital mortality in patients with cardiac injury (OR 2.01 [95% CI 1.28 – 3.15]) and in presence of altered echocardiography with RV dysfunction yielding a higher risk (OR 2.42 [95% CI 1.29 – 4.55]) compared with biventricular impairment (OR 1.86 [95% CI 0.87 – 4.00]) and isolated LV dysfunction (OR 1.30 [95% CI 0.77 – 2.19]) (Figure 2). Conclusion The use of echocardiography for the detection of cardiac dysfunction, has shown a greater correlation with mortality than the identification of acute cardiac damage using laboratory parameters. Of all the parameters obtained with the echocardiography, right ventricular dysfunction demonstrates the greatest correlation with mortality compared to left or biventricular dysfunction. However, the major cause of LV dysfunction in our population occurred during septic shock while RV dysfunction seemed to be due to pulmonary embolism and/or acute cor pulmonale ARDS-related.

29 Comparison between pure tachycardiomyopathy and acute heart failure and structural heart disease

Abstract Aims Tachycardiomyopathy (TCM) is a reversible cause of left ventricular dysfunction, secondary to rapid and/or asynchronous, irregular myocardial contraction. The disease can be divided in two main subgroups: arrhythmia-induced TCM also known as pure TCM, where the arrhythmia is the sole reason for the dysfunction, and impure TCM also known as arrhythmia mediated TCM, where the arrhythmia can exacerbate or worsen heart failure (HF) or an underlying heart disease. Pure TCM has already been described as affecting almost 1 out of 10 patients admitted for de novo acute HF. The aim of our study was to compare pure TCM and de novo acute HF and structural heart disease patients in terms of mortality and cardiovascular (CV)-related hospitalizations. Methods and results Prospective, observational study enrolling all consecutive patients with a confirmed diagnosis of TCM and all patients admitted for de novo acute HF. The TCM diagnosis was suspected in all patients admitted for HF-related symptoms, an ejection fraction &amp;lt;50% with concomitant persistent atrial or ventricular arrhythmia, and confirmed after clinical and echocardiographic recovery. Acute HF diagnosis was made in all patients with an ejection fraction &amp;lt;50%, new HF-like symptoms, diagnosis of structural heart disease and no evidence of clinical or echocardiographic recovery. For each patient, all-cause death and CV-related hospitalizations were recorded. One-hundred-and-ten patients with TCM (61.8% males, 68 ± 13 years old) were propensity matched with a control population of patients with HF and structural heart disease (76.6% males, 71 ± 15 years old, 75% ischaemic heart disease). After a median follow-up of 5.1 years (1st–3rd quartile 2.6–7.0 years) TCM patients showed an overall higher estimate of survival when compared to HF patients (78% vs. 58%; P = 0.031; Figure 1A) but a lower estimate of time free from CV-related hospitalization (31% vs. 57%, P = 0.014; Figure 1B). TCM patients got most often readmitted for AF-related elective procedures (60.8% of all hospitalizations) such ablation procedures or elective cardioversion, TCM recurrence (13.7%), and elective coronary angiography (5.9%). On the other hand, HF patients got readmitted for HF worsening (40.9%), cardiac or vascular surgery (22.7%), and elective coronary angiography (9.1%). Propensity-score matched analysis confirmed the results for all-cause death (81% vs. 49%; P = 0.006) and CV-related hospitalizations (29% vs. 54%; P = 0.007). Conclusions TCM is associated with higher rate of survival when compared to de novo acute HF, even after propensity score adjustment. On the other hand, patients with TCM got readmitted more frequently, requiring more often elective procedures in order to control the triggering arrhythmia.

Long-term prognosis of tachycardiomyopathy without underlying heart disease

Abstract Background Tachycardiomyopathy (TCM) is a reversible cause of left ventricular dysfunction, secondary to rapid and/or asynchronous, irregular myocardial contraction. Two categories of the disease have been described: arrhythmia-induced TCM (pure TCM), where the arrhythmia is the sole reason for the dysfunction, and arrhythmia-mediated TCM (impure TCM), where the arrhythmia can exacerbate or worsen heart failure (HF) or an underlying heart disease. Pure TCM has already been described as affecting almost 1 out of 10 patients admitted for acute HF-like symptoms. On the other side, acute HF leads to a chronic irreversible condition which tends to worsen over time and is burdened by a high rate of complications. Purpose The aim of our study was to compare pure TCM and de novo acute HF patients (including all forms of structural heart disease) in terms of mortality and cardiovascular (CV)-related hospitalizations. Methods Prospective, observational study enrolling all consecutive patients with a confirmed diagnosis of TCM and all patients admitted for de novo acute HF. The TCM diagnosis was suspected in all patients admitted for HF-related symptoms, an ejection fraction &amp;lt;50% with concomitant persistent atrial or ventricular arrhythmia, and confirmed after clinical and echocardiographic recovery. Acute HF diagnosis was made in all patients with an ejection fraction &amp;lt;50%, new HF-like symptoms, diagnosis of structural heart disease and no evidence of clinical or echocardiographic recovery. For each patient, all-cause death and CV-related hospitalizations were recorded. Propensity score matching was used in order to compare the two populations through sensitivity analysis. Results One-hundred-and-ten patients with TCM (61.8% males, 68±13 years old) were propensity matched with a control population of patients with HF and structural heart disease (76.6% males, 71±15 years old, 75% ischemic heart disease). After a median follow-up of 5.1 years (1st-3rd quartile 2.6–7.0 years) TCM patients showed an overall higher estimate of survival when compared to HF patients (78% vs. 58%; p=0.031; figure 1A) but a lower estimate of time free from CV-related hospitalization (31% vs. 57%, p=0.014; figure 1B). TCM patients got most often readmitted for AF-related elective procedures (60.8% of all hospitalizations), TCM recurrence (13.7%) and elective coronary angiography (5.9%). On the other hand, HF patients got readmitted for HF worsening (40.9%), cardiac or vascular surgery (22.7%) and elective coronary angiography (9.1%). Propensity-score matched analysis confirmed the results for all-cause death (81% vs. 49%; p=0.006) and CV-related hospitalizations (29% vs. 54%; p=0.007). Conclusions TCM is associated with a better survival when compared to de novo acute HF, even after propensity score adjustment. On the other hand, patients with TCM got readmitted more frequently, requiring more often elective procedures in order to control the triggering arrhythmia. Funding Acknowledgement Type of funding sources: None.

Predictors of left ventricular dysfunction in patients with Takayasu's arteritis: a single centre experience.

To determine the factors (clinical, biochemical, angiographic, and echocardiographic) which predict left ventricular (LV) dysfunction in Takayasu's arteritis (TAK). TAK causes inflammation of the aorta and its large branches. Systemic hypertension, aortic valvular disease, and coronary artery involvement are probable contributors to LV dysfunction in some patients. In other patients, inflammation and resulting myocarditis play an essential role. However, the prevalence and relative contribution of such predictors of LV dysfunction in TAK patients is unknown. We enrolled 87 patients with angiographically confirmed TAK in the study after proper informed consent. A complete clinical, biochemical, and echocardiographic evaluation of all the cases was done. We defined LV systolic dysfunction as an ejection fraction below 50% and diastolic dysfunction by ASE 2016 criteria into grades I, II, and III. We evaluated 87 consecutive angiographically proven TAK patients. The incidence of LV systolic and diastolic dysfunction in our study was 19.5% (17/87) and 100% (87/87), respectively. All the patients with LV dysfunction (n=17, 100%) had an ITAS 2010 score of more than two suggestive of active disease. In 15 (88%) out of 17 patients with LV systolic dysfunction, we could identify a significant haemodynamic cause of LV dysfunction (untreated hypertension HTN, descending thoracic or abdominal aorta stenosis, renal artery stenosis, coronary stenosis, significant valvular regurgitation). In the rest 2 cases, no important haemodynamic factor was present, and here LV dysfunction was probably because of myocarditis and its sequalae. This study represents the largest cohort of TAK patients to estimate LV systolic and diastolic dysfunction. We have found LV systolic and diastolic dysfunction multifactorial, with hemodynamic and inflammatory factors contributing to its pathophysiology.

Stroke Risk Following Takotsubo Cardiomyopathy.

Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is an increasingly recognized cause of left ventricular dysfunction. Previously considered a benign disease, Takotsubo cardiomyopathy may be a risk factor of ischemic stroke based on recent small, single-center case series. The strength and temporal profile of this association remains uncertain. We performed a cohort-crossover study using administrative claims data on all emergency department visits and acute care hospitalizations from 2005 to 2015 in California, New York, and Florida. We identified patients with Takotsubo cardiomyopathy, excluding those with a prior or concomitant stroke diagnosis. We compared the risk of ischemic stroke in the first year after Takotsubo cardiomyopathy to the risk of ischemic stroke in the second year after Takotsubo cardiomyopathy. Takotsubo cardiomyopathy and ischemic stroke were ascertained using previously validated ICD-9-CM codes. Absolute risks and odds ratios (OR) were calculated using McNemar test for matched data. Among 5283 patients with Takotsubo cardiomyopathy (mean age, 67 years; 92% female), we identified 49 ischemic strokes during the first year after Takotsubo cardiomyopathy versus 19 ischemic strokes during the second year after. The risk of stroke was significantly higher in the year after Takotsubo cardiomyopathy (absolute increase, 0.6%; 95% CI: 0.2-0.9; OR: 2.6; 95% CI: 1.5-4.6) as compared to the control period. We found a heightened risk of ischemic stroke in the year after a diagnosis of Takotsubo cardiomyopathy, although the absolute risk increase was small.

MON-LB041 Pheochromocytoma - Illusive Myriad of Symptoms

Background: Pheochromocytoma is a rare neuroendocrine neoplasm arising from the adrenal medullary chromaffin cells. It contributes to 80-85% of catecholamine secreting tumors. The annual incidence of pheochromocytoma is 0.8 cases per 100,000 person-years. It can be both sporadic or familial. The classic triad of headache, palpitations and diaphoresis is seen in only 4% of cases. Rare presentations include cardiomyopathy, stroke, diabetes mellitus, ventricular arrhythmias and myocardial infarction. Our patient presented concurrently with dilated cardiomyopathy, hypertensive emergency and new-onset diabetes mellitus (DM) followed by ischemic stroke within a week. Heart failure can present as takotsubo or dilated cardiomyopathy with an incidence of 10%. The underlying pathophysiology is catecholamine mediated myocardial stunning, diffuse coronary vasospasm, microvasculature dysfunction and fibrosis. DM is seen in 23% of pheochromocytoma and is due to catecholamine-induced impaired glucose tolerance, and insulin resistance. Cerebral ischemia has an incidence of 3%, and is secondary to severe hypertension and cerebral vasospasm. Clinical Case: A 47-year-old African American woman presented with a 1-week duration of worsening dyspnea, orthopnea, dizziness, and palpitations. Past medical history includes HTN, non-ischemic cardiomyopathy on carvedilol and pravastatin. Physical exam: BP 182/119, HR 120, mild pulmonary crackles. Labs: proBNP 3533 (1-150 pg/ml), HbA1c 13.1%. Echocardiogram: moderate global hypokinesis with left ventricle ejection fraction (LVEF) of 30-35%. On imaging, CT of chest revealed an incidental finding of 4.7 cm right adrenal adenoma. MRI abdomen confirmed heterogeneously enhancing 4.3 cm right adrenal mass. Further testing showed high plasma catecholamines of 9963 (242-1125 pg/ml), 24-hour urine catecholamines of 2125 (50-100 mcg), thus confirming the diagnosis of pheochromocytoma. Further, her clinical course was complicated by left-sided weakness. MRI brain reported an acute infarct in right corona radiata. Pre-operative blockade was done with phenoxybenzamine and metoprolol. Subsequently, she underwent right adrenalectomy and tissue diagnosis confirmed pheochromocytoma. On follow up visit, her symptoms resolved. Also noted normalized catecholamine levels, HbA1c of 5.4% and LVEF of 40- 45%. Conclusion: Pheochromocytoma can rarely present with multi-organ failure. It warrants a high index of suspicion in non-ischemic cardiomyopathy. As per recent Mayo Clinic criteria, diagnosis of takotsubo cardiomyopathy mandates ruling out pheochromocytoma. As seen in our patient, it is a reversible cause of left ventricular dysfunction, focal weakness and DM. Based on our knowledge, this is the only contingently diagnosed pheochromocytoma with varied clinical presentations. It has been aptly described as “The Great Masquerader”.

Terapia de resincronización cardiaca en paciente con miocardiopatía inducida por marcapasos.

Las complicaciones derivadas de la terapia de estimulación cardiaca tienen alta prevalencia, sin embargo, a menudo son olvidadas por el personal médico. La miocardiopatía secundaria a la disincronía biventricular por la alta carga de estimulación ventricular derecha es una causa frecuente de falla cardiaca, aumentando el riesgo de muerte, hospitalizaciones y disminuyendo la calidad de vida en los pacientes con marcapasos. Presentamos un caso de una paciente que desarrolló falla cardiaca, se descartaron las causas más comunes de disfunción ventricular izquierda y se consideró secundaria a miocardiopatía inducida por marcapasos, se le realizó cambio de dispositivo por terapia de resincronización cardiaca biventricular con adecuada respuesta clínica. Resaltamos la importancia de buscar en los pacientes con falla cardiaca complicaciones asociadas a dispositivos de estimulación ventricular derecha y considerar dentro del tratamiento el cambio a estimulación biventricular.

Diagnosing diabetic cardiomyopathy

Diabetic cardiomyopathy reflects the presence of structural or functional abnormalities of the myocardium in an individual with diabetes which are not fully explained by other factors known to cause myocardial dysfunction. Diabetes promotes a range of molecular and cellular changes leading to left ventricular concentric hypertrophy, fibrosis, abnormal perfusion, lipid deposition, altered metabolism, diastolic dysfunction, and later progression to systolic dysfunction. Diagnosis of diabetic cardiomyopathy requires identification of such pathological features whilst at the same time excluding other causes of left ventricular dysfunction. In this article, avail- able modalities which can contribute to a diagnosis of diabetic cardiomyopathy are discussed. In most cases a diagnosis of diabetic cardiomyopathy can be reached by echocardiography or cardiac magnetic resonance imaging to detect structural and functional myocardial changes, with computed tomography coronary angiography being employed to exclude obstructive coronary artery disease which could account for left ventricular dysfunction.

Mirror image: Recurrent Takotsubo cardiomyopathy with variable regional involvement

Takotsubo cardiomyopathy (TCM), a stress-induced cardiomyopathy, is a well-recognised cause of left ventricular dysfunction. It commonly presents similar to acute coronary syndrome with chest, dyspnoea, and electrocardiographic changes consistent with ischaemia and elevations of cardiac markers. Takotsubo cardiomyopathy often presents with acute myocardial stunning without evidence of coronary artery disease or atherosclerotic disease that is out of proportion to the demonstrated disease. Takotsubo cardiomyopathy has characteristic left ventriculography and radiographic findings – including left ventricular hypokinesis, adjacent areas of hyperkinesis, and variable regional involvement (i.e. apical, mid-ventricular, or basal ballooning patterns). Recurrent disease can occur and is often found to have similar ventricular wall dysfunction patterns. However, we present an uncommon case of possible recurrent Takotsubo cardiomyopathy that was found to have variable regional involvement.

Unusual cause of left ventricular dysfunction in a child

Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery is a rare congenital heart disease and a cause of myocardial ischemia during childhood. Most undiagnosed cases die in the first year of life as an extensive collateral network is essential for survival. The diagnosis requires a high index of clinical suspicion. The authors present the case of an 8-year-old black asymptomatic child referred from Cape Verde Island in order to clarify left ventricular dilatation and dysfunction with systo-diastolic turbulent flows observed at the interventricular septum. At the age of 3 months, she was diagnosed with heart failure, in the context of showing dilated cardiomyopathy. She was managed and clinically improved with anticongestive therapy, which she was still taking at the time of admission to our Center. The echocardiogram findings suggested Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery and the diagnosis was confirmed by computerized angiotomography and cardiac catheterization. The patient was successfully submitted to direct implantation of the left coronary artery into the aorta, allowing the creation of a double coronary perfusion system. This case illustrates an unusual presentation of a rare pathology that survived without a diagnosis after the first year of life. It also reinforces the importance of multimodality image screening in these cases.

Abstract TP212: Stroke Risk Following Takotsubo Cardiomyopathy

Introduction: Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is an increasingly recognized cause of left ventricular dysfunction after acute brain injury. Previously considered a benign disease, recent small, single-center case series suggest that Takotusubo cardiomyopathy may be a risk factor for ischemic stroke. The strength and temporal profile of this association remain uncertain. Methods: We performed a cohort-crossover study using administrative claims data on all emergency department visits and acute care hospitalizations from 2005-2015 in California New York, and Florida. We identified patients with Takotsubo cardiomyopathy using a previously validated International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis code. We excluded patients with a prior or concomitant stroke diagnosis. We compared the risk of ischemic stroke in the first year after Takotsubo cardiomyopathy to the risk of ischemic stroke in the second year after. The absolute risk increase and odds ratio (OR) were calculated using McNemar’s test for matched data. Results: Among 5,283 patients with Takotsubo cardiomyopathy (mean age, 67 years; 92% female), we identified 49 ischemic strokes during the year after Takotsubo cardiomyopathy versus 19 ischemic strokes in the control period 2 years later. The risk of stroke was significantly higher in the year after Takotsubo cardiomyopathy (absolute increase, 0.6%; 95% CI, 0.2%-0.9%) (OR, 2.6; 95% CI, 1.5-4.6) as compared to the control period. Conclusion: We found a heightened risk of ischemic stroke in the year after a diagnosis of Takotsubo cardiomyopathy, although the absolute risk increase was small.

Right ventricular apical pacing induced left ventricular systolic dysfunction

Right ventricular apical pacing remained the conventional pacing site for the cardiologists from beginning. But studies later on confirmed that long term right ventricular pacing is a cause of left ventricular dysfunction even in patients with pre pacemaker implantation normal LV ejection fraction. Some observational studies and small RCTs also analyzed the predictors of LV dysfunction. In current scenario main focus is on alternate more physiological pacing site, like RVOT pacing and to enable some special algorhythms that decrease the total percentage of the pacing. Thus it is Important to understand the mechanism of post RV apical pacing LV dysfunction, other predictors of LV dysfunction and how to treat/prevent the LV dysfunction.

An Updated Systematic Review and Meta-analysis of the Short- and Long-term Outcomes of Percutaneous Coronary Intervention for Patients with Severe Left Ventricular Systolic Dysfunction

Background: Coronary artery disease (CAD) is the most common cause of left ventricular dysfunction (LVD). Confl icting evidence exists with regards to available treatments and patient prognosis. Revascularization may improve ventricular function while coronary artery bypass surgery (CABG) has signifi cantly improved survival. The effectiveness of percutaneous coronary intervention (PCI) has also not been thoroughly investigated to date.

Ejection fraction in left bundle branch block is disproportionately reduced in relation to amount of myocardial scar

IntroductionThe relationship between left ventricular (LV) ejection fraction (EF) and LV myocardial scar can identify potentially reversible causes of LV dysfunction. Left bundle branch block (LBBB) alters the electrical and mechanical activation of the LV. We hypothesized that the relationship between LVEF and scar extent is different in LBBB compared to controls. MethodsWe compared the relationship between LVEF and scar burden between patients with LBBB and scar (n = 83), and patients with chronic ischemic heart disease and scar but no electrocardiographic conduction abnormality (controls, n = 90), who had undergone cardiovascular magnetic resonance (CMR) imaging at one of three centers. LVEF (%) was measured in CMR cine images. Scar burden was quantified by CMR late gadolinium enhancement (LGE) and expressed as % of LV mass (%LVM). Maximum possible LVEF (LVEFmax) was defined as the function describing the hypotenuse in the LVEF versus myocardial scar extent scatter plot. Dysfunction index was defined as LVEFmax derived from the control cohort minus the measured LVEF. ResultsCompared to controls with scar, LBBB with scar had a lower LVEF (median [interquartile range] 27 [19–38] vs 36 [25–50] %, p < 0.001), smaller scar (4 [1–9] vs 11 [6–20] %LVM, p < 0.001), and greater dysfunction index (39 [30–52] vs 21 [12–35] % points, p < 0.001). ConclusionsAmong LBBB patients referred for CMR, LVEF is disproportionately reduced in relation to the amount of scar. Dyssynchrony in LBBB may thus impair compensation for loss of contractile myocardium.

The Prognostic Factors of Alcoholic Cardiomyopathy: A single-center cohort study.

Background:Alcoholic cardiomyopathy (ACM) is considered one of the main causes of left ventricular dysfunction and is the leading cause of nonischemic dilated cardiomyopathy (DCM) in developed countries. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM.Aims:This study aimed to identify risk factors related to a poor outcome in ACM patients.Study design:Retrospective cohort study.Methods:This study included 321 patients with ACM admitted to our hospital between 2003 and 2013. This study aimed to investigate the clinical characteristics and outcomes of the patients with ACM, and the primary endpoint of the study was all-cause mortality, which was assessed through patient medical records (review of patient hospital records and periodic examination of patients in the outpatient clinic) and medical follow-up calls with trained personnel. All-cause mortality was assessed using Kaplan–Meier survival curves, and the risk factors were assessed using Cox regression. A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups.Results:After a median follow-up period of 3.78 years (interquartile range: 2.08–6.52 years), 83 (27.7%) patients were dead. The independent predictors of all-cause mortality due to ACM were the QRS duration (HR: 1.014; 95% CI: 1.004–1.019; P = .003), systolic blood pressure (HR: 0.980; 95% CI: 0.963– 0.997; P = .020), and New York Heart Association classification (HR: 1.595; 95% CI: 1.110–2.290; P = .011) at admission.Conclusion:Our study indicated that the QRS duration, systolic blood pressure, and New York Heart Association classification at admission provided independent prognostic information in patients with ACM.

Spinal Cord Injury Causes Systolic Dysfunction and Cardiomyocyte Atrophy.

Individuals with spinal cord injury (SCI) have been shown to exhibit systolic, and to a lesser extent, diastolic cardiac dysfunction. However, previous reports of cardiac dysfunction in this population are confounded by the changing loading conditions after SCI and as such, whether cardiac dysfunction per se is present is still unknown. Therefore, our aim was to establish if load-independent cardiac dysfunction is present after SCI, to understand the functional cardiac response to SCI, and to explore the changes within the cellular milieu of the myocardium. Here, we applied in vivo echocardiography and left-ventricular (LV) pressure-volume catheterization with dobutamine infusions to our Wistar rodent model of cardiac dysfunction 5 weeks following high (T2) thoracic contusion SCI, while also examining the morphological and transcriptional alterations of cardiomyocytes. We found that SCI significantly impairs systolic function independent of loading conditions (end-systolic elastance in control: 1.35 ± 0.15; SCI: 0.65 ± 0.19 mm Hg/μL). The reduction in contractile indices is accompanied by a reduction in width and length of cardiomyocytes as well as alterations in the LV extracellular matrix. Importantly, we demonstrate that the reduction in the rate (dP/dtmax) of LV pressure rise can be offset with beta-adrenergic stimulation, thereby experimentally implicating the loss of descending sympatho-excitatory control of the heart as a principle cause of LV dysfunction in SCI. Our data provide evidence that SCI induces systolic cardiac dysfunction independent of loading conditions and concomitant cardiomyocyte atrophy that may be underpinned by changes in the genes regulating the cardiac extracellular matrix.