Reversible Left Ventricular Dysfunction Research Articles

Impact of left bundle branch block in patients with takotsubo cardiomyopathy

Abstract Background Takotsubo cardiomyopathy (TCM) is a syndrome characterized by reversible left-ventricular regional systolic dysfunction in the absence of obstructive coronary artery disease (CAD). The presence of left bundle branch block (LBBB) has been described as an independent predictor of mortality in patients with CAD. One study using the National Inpatient Sample (NIS) for 2016 found that the presence of LBBB was associated with worse outcomes in patients with TCM. Purpose To better clarify the association between LBBB and various in-hospital outcomes in patients with TCM. Methods The NIS database was queried from 2016–2019 to identify all admissions with a primary diagnosis of TCM that had a cardiac catheterization to improve the specificity of the diagnosis. International classification of diseases, tenth revision clinical modification (ICD-10-CM) codes were used to divide patients based on the presence or absence of LBBB. A 1:3 propensity score matching based on age, race, gender, and risk factor stratification was used to reduce selection bias. Multivariate linear and logistic regression analysis was performed to compare various outcomes among both groups. Results A total of 27,125 patients admitted with a primary diagnosis of TCM that also underwent diagnostic coronary angiography were identified. In the study sample, 955 (3.5%) were determined to have a LBBB. After calculating propensity scores, 955 patients with LBBB were paired to 2,865 patients without LBBB. LBBB was associated with higher rates of ventricular arrhythmias (AOR=3.098, 95% CI 1.483–6.471, p=0.003); however, it was not statistically associated with cardiogenic shock, sudden cardiac arrest (SCA), acute kidney injury, acute heart failure, and hospital length of stay. In addition, there was no statistical difference in intra-hospital mortality. Conclusions LBBB is associated with left ventricular dyssynchrony. It has been proposed that intraventricular dyssynchrony might be a predisposing factor for ventricular arrhythmias (VA) and SCA. Several trials have demonstrated that cardiac resynchronization therapy alone (i.e., without defibrillation) reduces the rate of VA and SCA. The mechanism for this improvement is unclear but may be related to hemodynamic improvement from ventricular synchrony in heart failure (HF). In fact, LBBB has been reported as an independent risk factor for all-cause mortality and SCA at one year in patients with HF. Our analysis did not find any significant association between LBBB and SCA but did find an association with VA. Moreover, there were not enough events of intra-hospital mortality to assess a possible association between LBBB and mortality. Therefore, a prospective study with a longer follow-up would be needed to clarify the role of LBBB in mortality and establish causality between LBBB and VA in patients with TCM. Funding Acknowledgement Type of funding sources: None.

SEVERITY OF LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH TACHYCARDIA-INDUCED CARDIOMYOPATHY: IMPACTS ON REMODELING AFTER ATRIAL FLUTTER ABLATION

Tachycardia-induced cardiomyopathy (TIC) is defined as a reversible systolic left ventricular (LV) dysfunction resulting from an elevated heart rate. It has been reported in patients with incessant or very frequent tachyarrhythmias, including atrial flutter. However, little is known about the evolution of LV remodeling in these patients, especially when severe LV dysfunction is present at diagnosis. Hence, the objectives of this study were to evaluate the proportion of severe LV dysfunction, and to describe the timing of LV recovery after atrial flutter ablation in patients with a presumed TIC.

A Review of Nuclear Imaging in Takotsubo Cardiomyopathy.

Takotsubo cardiomyopathy or Takotsubo Syndrome (TTS) is a reversible left ventricular dysfunction syndrome that is increasingly being recognized. Recent advances in nuclear imaging have allowed us to study TTS in greater detail. We searched the PubMed and Medline databases and identified 53 publications with 221 patients reporting nuclear imaging findings in TTS. The age of the patients ranged from 17 to 87 years and were predominantly women (88.2%). The TTS variant was apical (typical) in 170 (76.9%), mid-ventricular in 23 (10.4%), and basal (reverse TTS) in 2 (0.9%). Cardiac perfusion was assessed using 99mTc sestamibi (MIBI) SPECT, 99mTc tetrofosmin SPECT, 201Tl SPECT, 82Rb PET, 201Tl SPECT, and 13N ammonia PET. Additional studies used were 123I MIBG SPECT, 123I BMIPP SPECT, 18F FDG PET, 67Ga citrate, and 11C hydroxy-ephedrine. A perfusion defect was seen in 69 (31.2%), and an inverse perfusion–metabolism mismatch (normal or near-normal perfusion with absent myocardial metabolic activity) was seen in 183 (82.8%) patients. Nuclear imaging has a significant role in evaluating, diagnosing, and prognosticating patients with TTS. As nuclear imaging technology evolves, we will surely gain more insights into this fascinating disorder.

Tachycardiomyopathy entails a dysfunctional pattern of interrelated mitochondrial functions

Tachycardiomyopathy is characterised by reversible left ventricular dysfunction, provoked by rapid ventricular rate. While the knowledge of mitochondria advanced in most cardiomyopathies, mitochondrial functions await elucidation in tachycardiomyopathy. Pacemakers were implanted in 61 rabbits. Tachypacing was performed with 330 bpm for 10 days (n = 11, early left ventricular dysfunction) or with up to 380 bpm over 30 days (n = 24, tachycardiomyopathy, TCM). In n = 26, pacemakers remained inactive (SHAM). Left ventricular tissue was subjected to respirometry, metabolomics and acetylomics. Results were assessed for translational relevance using a human-based model: induced pluripotent stem cell derived cardiomyocytes underwent field stimulation for 7 days (TACH–iPSC–CM). TCM animals showed systolic dysfunction compared to SHAM (fractional shortening 37.8 ± 1.0% vs. 21.9 ± 1.2%, SHAM vs. TCM, p < 0.0001). Histology revealed cardiomyocyte hypertrophy (cross-sectional area 393.2 ± 14.5 µm2 vs. 538.9 ± 23.8 µm2, p < 0.001) without fibrosis. Mitochondria were shifted to the intercalated discs and enlarged. Mitochondrial membrane potential remained stable in TCM. The metabolite profiles of ELVD and TCM were characterised by profound depletion of tricarboxylic acid cycle intermediates. Redox balance was shifted towards a more oxidised state (ratio of reduced to oxidised nicotinamide adenine dinucleotide 10.5 ± 2.1 vs. 4.0 ± 0.8, p < 0.01). The mitochondrial acetylome remained largely unchanged. Neither TCM nor TACH–iPSC–CM showed relevantly increased levels of reactive oxygen species. Oxidative phosphorylation capacity of TCM decreased modestly in skinned fibres (168.9 ± 11.2 vs. 124.6 ± 11.45 pmol·O2·s−1·mg−1 tissue, p < 0.05), but it did not in isolated mitochondria. The pattern of mitochondrial dysfunctions detected in two models of tachycardiomyopathy diverges from previously published characteristic signs of other heart failure aetiologies.

Takotsubo syndrome in New Zealand: current knowledge and future challenges.

Takotsubo syndrome (TS), also known as apical ballooning syndrome, is a transient stress-related cardiomyopathy characterised by acute but reversible left ventricular dysfunction. The condition tends to occur in postmenopausal women after a stressful event. At presentation, TS typically mimics acute myocardial infarction (MI) and the incidence of TS has been increasing worldwide. This is likely a consequence of an improved awareness of the existence of this syndrome and easier access to early echocardiography and coronary angiography. However, its aetiology remains poorly understood and it is probably still underdiagnosed. Similar to other countries, TS is being increasingly recognised in New Zealand. In this review, we discuss the demographics, clinical features and outcomes of patients with TS in New Zealand. Doing so informs us not only of the pattern of disease in New Zealand but it also provides insights into the condition itself.

Takotsubo сardiomyopathy: case report

Stress-induced cardiomyopathy, also known as takotsubo cardiomyopathy (TCM), is a type of reversible left ventricular dysfunction that occurs after emotional or physical stress and manifests as chest pain, electrocardiographic changes mimicking myocardial ischemia, cardiac enzyme elevation, transient left ventricular dysfunction involving mid and apical segments and normal or near-normal coronary angiography. This syndrome could happen after iatrogenic stressors like anesthesia or surgery. We hereby present two cases of TCM after anesthesia and surgery. In both cases, clinical, electrocardiographic, echocardiographic, and angiographic findings are employed to confirm this diagnosis.

A Clinical Case of Takotsubo Syndrome in the Early Postoperative Period of Rhinoplasty

Takotsubo syndrome (TS) is an acute reversible left ventricular myocardial dysfunction caused by an emotional or physical trigger. In the perioperative period, TS is in some cases induced by various psychological factors, such as stress before/after surgery, and non-psychological factors, such as drug administration. This article describes the clinical observation of takotsubo syndrome that developed in the early postoperative period of rhinoplasty

P312 A CASE OF TAKOTSUBO CARDIOMYOPATHY IN SARS–COV–2 INFECTION

Cardiovascular complications are a frequent occurrence in Sars–CoV–2 infection. Takotsubo cardiomyopathy is a possible cause of transient ST segment elevation (1–3% of total cases) and is characterized by a reversible left ventricular dysfunction with coronary arteries free from critical stenosis. The predominant echocardiographic pattern is an akinesia of the mid–apical myocardial segments with preserved kinetics of the basal segments. The incidence of Takotsubo cardiomyopathy showed a marked increase during the COVID–19 pandemic. Three factors mainly contribute to the onset of cardiomyopathy in patients with COVID–19: cytokine storm, adrenergic hyperactivation and microvascular dysfunction. A 79–year–old woman was hospitalized in the Pneumology department of our hospital for bilateral interstitial pneumonia Sars–CoV–2 related. In remote medical history: in 2010 diagnosis of breast cancer with negative follow–up for disease recovery, arterial hypertension, hypercholesterolemia and syndrome of reduced mobility as a result of a previous ischemic stroke. Non–invasive mechanical ventilation with c–PAP was started and, for the detection of anterolateral electrocardiographic anomalies (diffuse symmetrical negative T waves) and an increase in myocardionecrosis markers, echocardiographic evaluation was performed, which revealed an akinesia of the mid–apical segments of the left ventricle with preserved kinetics of the basal segments and severely depressed global systolic function (ejection fraction: 30%). BNP (18.100 pg /mL), interleukin–6 (339 pg /mL) and CRP (136 mg /L) were elevated on blood chemistry tests. In the suspicion of Takotsubo cardiomyopathy (InterTAK Score: 67, probability: 79.8%), cardioprotective therapy with ACE inhibitor, beta–blocker, diuretics, low molecular weight heparin, double antiaggregation and statin was started, deferring coronary angiography to improved clinical conditions. In the following days, due to the respiratory and haemodynamic worsening, the patient was transferred to an intensive setting, where she was intubated and treated with levosimendan and noradrenaline. Serial echocardiograms showed a progressive improvement of the global systolic function (ejection fraction at the last checkup: 55%), with complete regression of the kinetic anomalies, confirming of the diagnostic hypothesis of stress cardiomyopathy. For a pulmonary mycotic superinfection, complicated by iatrogenic pneumothorax, in the following days the patient died.

P141 CORRELATION BETWEEN TAKO–TSUBO SYNDROME AND OCCULT CANCER

Abstract Introduction Tako–Tsubo Syndrome (“TTS”) is a cardiomyopathy characterized by an acute reversible left ventricular dysfunction, mainly triggered by emotional or physical stress. Several variants have been reported, including reverse TTS, characterized by hypokinesia of basal segments and hyperkinesis of the apical ones. TTS has a clinical presentation similar to acute coronary syndrome but without evidence of obstructive coronary artery disease. A surprising association between TTS and cancer arose out of recent studies. Case Presentation 74–year–old patient got to the emergency room of our hospital for the appearance, apparently in the health, in the absence of physical or emotional stress of oppressive chest pain. On the ECG, there was evidence of ST–segment elevation in inferior leads, for which urgent coronary angiography was performed. It did not show significant stenotic lesions nor evidence of elevated troponin values. The Echocardiogram showed hypokinesia of the basal segments and hyperkinesis of the mid–apical ones, with EF 40%. In the following days, the patient performed MRI–heart with detection of LGE of the intramyocardial type (non–ischemic pattern) in correspondence with the inferior wall in the medioventricular area. During hospitalization on routine chest x–ray, hypodiaphanous image was found in the left apex for which an HR CT scan of the chest was performed which a lesion in the left apical lung area with spiculated margins of a heteroplastic nature, associated with multiple bilateral lesions suggestive of secondaryism. Therefore, the patient was taken over by the Oncology service. Conclusions Such case confirms the association between TTS and occult cancer. In the absence of obvious physical or emotional stress that may explain the onset of TTS, it is important to research for any silent neoplastic pathology. The literature shows that the prevalence of malignant diseases is high in patients with TTS. Recent studies have pinpointed the activation of the sympathetic nervous system promotes cardiac inflammation by upregulating ICAM–1 and the expression of p53. Furthermore, inflammation can lead to the activation of p38 MAP Kinase, thus contributing to myocardial stunning. The specific role of inflammation as a cofactor of adrenaline–induced stunning deserves further investigation in the specific context of malignant tumors, which are frequently associated with an enhanced inflammatory state.

Preservation of Right Ventricular Contractility After Transient Phenylephrine‐Induced Pressure Overload in Swine

ObjectiveWe have previously demonstrated that a transient phenylephrine (PE)‐induced rise in systemic arterial blood pressure leads to reversible left ventricular (LV) systolic dysfunction in the absence of ischemia (i.e., “stretch‐induced stunning”). However, the extent to which this phenomenon occurs in the right ventricle (RV) is unclear. Accordingly, the present study was designed to assess changes in pulmonary artery (PA) pressure and RV function during and after systemic administration of PE in swine.MethodsClosed‐chest propofol‐anesthetized swine (n=5) were instrumented with a Swan‐Ganz catheter and an admittance catheter for continuous measurement of PA pressure, RV pressure, and RV volume (ADV500; Transonic SciSense, Inc.). Ventricular end‐diastolic and end‐systolic volumes were assessed by multi‐detector computed tomography with iodinated contrast (1 mL/kg at 4 mL/s) before, during, and 30‐minutes after transient pressure overload elicited by a 1‐hour intravenous infusion of PE (18 mg/hour). Load‐independent RV systolic function was derived from RV pressure‐volume loops collected during inferior vena cava occlusion at baseline and 30 min after PE.ResultsPE elicited a significant rise in PA pressure (27±1/14±1 to 43±1/23±31mmHg; p&lt;0.05) and RV pressure (25±2/3±1 to 44±2/8±2 mmHg; p&lt;0.05) that normalized 30‐minutes after the end of the infusion period (PA: 28±1/11±1 mmHg; RV: 29±5/4±2 mmHg). This was accompanied by a significant increase in RV end‐diastolic and end‐systolic volumes and decrease in RV ejection fraction that tended to persist 30‐minutes after cessation of PE (Table; top panel). However, load‐dependent (dP/dtmax) and load‐independent (ESPVR and PRSW) parameters of RV systolic function were preserved after PE‐induced TPO (Table; bottom panel).ConclusionsDespite causing a significant rise in RV preload volume and pressure, transient PE‐induced pressure overload is not associated with RV contractile dysfunction during the post‐infusion period. The absence of stretch‐induced stunning in the RV may be linked to inherent differences in compliance relative to the LV as well as a diminished pressor response to PE in the pulmonary vs. systemic circulation.

Stretch‐induced Myocardial Injury and Inflammation After Transient Vasopressin‐Mediated Left Ventricular Pressure Overload in Swine

ObjectiveUsing the α1‐adrenergic agonist phenylephrine (PE), we have previously demonstrated that an acute episode of transient pressure overload (TPO) elicits stretch‐induced myocardial injury and reversible left ventricular (LV) systolic dysfunction. Although this was accompanied by leukocyte mobilization, a rise in inflammatory cytokine levels, and increased pro‐inflammatory gene expression in the heart, the extent to which this resulted from direct activation of α1‐adrenergic receptors on immune cells vs. an inflammatory response to mechanical stretch‐induced myocardial injury is unclear. Accordingly, the present study was designed to determine if an inflammatory response to myocardial injury is evident when TPO is produced by vasopressin (VP), a vasoconstrictor without direct α1‐adrenergic agonist properties.MethodsHemodynamic and echocardiographic parameters were assessed in propofol‐anesthetized swine before, during, and after a 30‐minute infusion of VP (VP‐TPO; 0.04 U/kg/min, n=7) to increase LV end‐diastolic pressure (EDP) to ~30mmHg. Serial jugular venous blood sampling was performed to quantify circulating cardiac troponin I (cTnI), leukocytes, and inflammatory cytokines (TNF‐α and IL‐6) at baseline and 3‐hours after cessation of VP‐TPO. Leukocyte and cytokine levels were compared with those observed after PE‐mediated TPO in a separate group of animals (PE‐TPO; n=6).ResultsVP elicited a significant rise in mean arterial pressure (91±5 to 165±11 mmHg) and LV EDP (10±1 to 29±2 mmHg; both p&lt;0.05 vs. baseline). This was accompanied by a significant rise in LV end‐diastolic volume (73±5 to 110±7 mL) and end‐systolic volume (20±3 to 53±6 mL), as well as a reduction in LV ejection fraction (EF; 72±3 to 52±3 %; all p&lt;0.05 vs. baseline). One hour after cessation of VP‐TPO, LV EF remained depressed vs. baseline (60±3 %; p&lt;0.05) and circulating cTnI levels began to rise, reaching a concentration that was ~10‐fold higher than baseline concentrations at the 3‐hour post‐TPO timepoint (18±5 to 118±21 ng/L; p&lt;0.05). These changes were accompanied by a significant rise in circulating neutrophils, monocytes, TNF‐α, and IL‐6 that was similar to that observed after PE‐TPO (Figure).ConclusionsVP‐TPO elicits myocardial injury, leukocyte mobilization, and an acute rise in circulating pro‐inflammatory cytokines, thereby recapitulating several features of PE‐TPO in the absence of direct α1‐adrenergic stimulation. These findings suggest that stretch‐induced myocardial injury provokes an inflammatory response that may play an important role in promoting the development of cardiac fibrosis and diastolic dysfunction after exposure to repetitive episodes of TPO.

Takotsubo Syndrome from Coronavirus Disease 2019

Takotsubo syndrome (TTS) or stress-induced cardiomyopathy is a rare form of acute, reversible left ventricular dysfunction. Catecholaminergic surge, myocardial inflammation, impaired microvascular perfusion, and electrophysiologic derangements may all contribute to its clinical manifestations of myocardial stunning and apical ballooning.1

Mechanisms of Myocardial Stunning in Stress-Induced Cardiomyopathy

Stress-induced cardiomyopathy, in contrast to acute myocardial infarction, is a type of acute heart failure characterized by reversible left ventricular dysfunction. Cardiac imaging primarily reveals left ventricle myocardial stunning, 81.7% of which is apical type. Emotional or psychological stress usually precedes the onset of stress-induced cardiomyopathy, which is increasingly being recognized as a unique neurogenic myocardial stunning disease. To distinguish between acute myocardial infarction and acute viral or auto-immune myocarditis, this review summarizes specific mechanisms of myocardial stunning in stress-induced cardiomyopathy, such as calcium disorders, metabolic alterations, anatomical and histological variations in different parts of the left ventricle, and microvascular dysfunction.

The influence of summer temperatures on the incidence of Takotsubo cardiomyopathy : a retrospective study

Takotsubo cardiomyopathy (TK-CM) is a reversible acute left ventricular dysfunction that cannot be explained by an obstructive coronary lesion. The aim of our study was to explore the possible correlation between the incidence of TK-CM in summer and the average temperature, number of heat waves or number of days hotter than 30°C. 482 patients presented an acute coronary syndrome in the summers of 2012 until 2017 in our region. 15 patients met the inclusion and exclusion criteria and were diagnosed as TK-CM. The study analysis showed a statistically correlation between the number of heatwaves and the incidence of TK-CM (coefficient of correlation: 0.77; p = 0.04). This comforts the hypothesis of climatic influence on this pathology.

474 A case of Takotsubo cardiomyopathy in SARS-CoV-2 infection

Cardiovascular complications are a frequent occurrence in SARS-CoV-2 infection. Takotsubo cardiomyopathy (also known as stress cardiomyopathy) is a possible cause of transient ST segment elevation (1–3% of total cases) and is characterized by a reversible left ventricular dysfunction with coronary arteries free from critical stenosis. The predominant echocardiographic pattern of this cardiomyopathy is an akinesia of the mid-apical myocardial segments (‘apical ballooning’), with preserved kinetics of the basal segments. The incidence of Takotsubo cardiomyopathy showed a marked increase during the COVID-19 pandemic. The data showed that three factors mainly contribute to the onset of cardiomyopathy in patients with COVID-19: cytokine storm, adrenergic hyperactivation and microvascular dysfunction. A 79-year-old woman was hospitalized in the Pneumology department of our hospital for acute hypoxemic respiratory failure due to bilateral interstitial pneumonia SARS-CoV-2 related. In remote medical history: in 2010 diagnosis of breast cancer, treated with quadrantectomy, adjuvant chemo- and radiotherapy, with negative follow-up for disease recovery, systemic arterial hypertension, hypercholesterolaemia and from 2016 syndrome of reduced mobility as a result of a previous ischaemic stroke. Non-invasive mechanical ventilation with c-PAP was started in the ward and, for the detection of anterolateral electrocardiographic anomalies (diffuse symmetrical negative T waves. Figure) and an increase in myocardionecrosis markers (troponin I peak: 5.4 ng/ml), in the absence of chest pain or equivalent, echocardiographic evaluation was performed, which revealed an akinesia of the mid-apical segments of the left ventricle with preserved kinetics of the basal segments and severely depressed global systolic function (ejection fraction: 30%). BNP (18.100 pg/ml), interleukin-6 (339 pg/ml), and CRP (136 mg/l) were elevated on blood chemistry tests. In the suspicion of Takotsubo cardiomyopathy (InterTAK Score: 67, probability: 79.8%), cardioprotective therapy with ACE inhibitor, beta-blocker, diuretics, low molecular weight heparin, double antiaggregation, and statin was started, deferring coronary angiography to improve clinical conditions. In the following days, due to the respiratory and haemodynamic worsening, the patient was transferred to an intensive setting, where she was intubated and treated with levosimendan and noradrenaline. In the intensive care unit, serial echocardiograms (over 30 days) showed a progressive improvement, up to normalization, of the global systolic function (ejection fraction at the last checkup: 55%), with complete regression of the kinetic anomalies, confirming the diagnostic hypothesis of stress cardiomyopathy. For a pulmonary mycotic superinfection (positive bronchoaspirate for Candida albicans and Candida krusei), complicated by iatrogenic pneumothorax, in the following days the patient died.

180 Cognitive disorders in takotsubo syndrome: incidence, short, and long term outcome. Results from a prospective multi-centre registry

Abstract Aims Takotsubo syndrome (TTS) is an acute and reversible left ventricular dysfunction, whose pathophysiological mechanisms are not completely known. There are evidence suggesting a possible link between neurological disease and TTS. Aim of the study was to evaluate incidence and prognostic value of cognitive neurological disorders among TTS patients. Methods and results 379 consecutive patients were enrolled in a prospective multicentre registry. History, clinical features, echocardiographic parameters, in-hospital complications and long-term Follow-up events of all patients were recorded. Cognitive neurological disorders included Alzheimer disease, old age dementia and cognitive impairment for other causes. Prevalence of cognitive neurological disorders among TTS patients was 5.5% (num = 21). Among this subset of patients 48% (num = 10) had Alzheimer syndrome, 24% (num = 5) old age dementia and 28% (num = 6) cognitive impairment for other causes. Compared to the control group, these patients were older (81 ± 5 vs. 71 ± 12, P = 0.01) and predominantly men (24% vs. 9%, P = 0.01). No differences in term of cardiovascular risk factors and left ventricular ejection fraction at admission and discharge were found among the two groups. TTS patients with cognitive neurological disorders experienced higher rate of in-hospital complications (62% vs. 28%, P = 0.01), that were mainly driven by higher rate of pulmonary oedema (14% vs. 9%, P = 0.01), cardiogenic shock (29% vs. 8%, P = 0.01), death (24% vs. 4% P = 0.01), ischaemic stroke (10% vs. 4%, P = 0.01), and left ventricular thrombi (10% vs. 3%, P = 0.01). At long-term follow-up patients with cognitive neurological disorders when compared to those without, experienced higher rate of mayor cardiovascular events (48% vs. 16%, P = 0.01), cardiovascular re-hospitalization (14% vs. 10%, P = 0.01) and death (43% vs. 9%, P = 0.01). Conclusions TTS patients with cognitive neurological disorders had an increased risk of in and out of hospital mayor cardiac adverse events and mortality at short and long-term follow-up.

Presumptive and reversible left ventricular systolic dysfunction secondary to chloramphenicol administration in a dog

AbstractA 6‐year‐old neutered male 35 kg Staffordshire terrier dog was presented for evaluation of interdigital furunculosis. Culture from lesions revealed meticillin‐resistant Staphylococcus pseudintermedius, with susceptibility to only amikacin, chloramphenicol and vancomycin. Chloramphenicol was administered at a dose of 1500 mg orally every 8 hours (42 mg/kg) for a total of 52 days. On Day 52 of treatment, a new mid‐systolic click was appreciated on cardiothoracic auscultation that prompted cardiac evaluation. Echocardiogram revealed mild mitral valve prolapse with no mitral valve regurgitation and mild left ventricular systolic dysfunction in multiple indices. Chloramphenicol was discontinued, and a recheck echocardiogram performed 63 days later showed persistent mild mitral valve prolapse and resolution of the left ventricular systolic dysfunction. Reversible left ventricular systolic dysfunction should be considered a potential complication associated with chloramphenicol therapy, and suggests chloramphenicol may need to be used with caution in canine patients with underlying cardiac disease.

Electrocardiographic Changes in a Man With Acute Pancreatitis: A Myocardial Infarction?

A 69-year-old man with a history of heavy alcohol use presented with abdominal pain and was diagnosed with alcohol-induced acute pancreatitis. On admission, he had not reported chest pain, palpitations, or dyspnea. Initial laboratory tests showed a lactic acid level of 8.3 mmol/L (normal, 0.5–2.2 mmol/L), normal renal function, and normal cardiac enzyme levels. An electrocardiogram (ECG) on admission showed sinus tachycardia. His symptoms and lactic acidosis resolved after aggressive fluid resuscitation and bowel rest. Two days later, sudden-onset dyspnea, tachycardia, and hypoxia necessitated the administration of 2 L of supplemental oxygen. A chest radiograph showed acute pulmonary edema. The patient's serum cardiac troponin level peaked at 0.35 ng/mL (normal, &lt;0.03 ng/mL), and his brain natriuretic peptide level was 235 pg/mL (normal, &lt;100 pg/mL). His ECG showed changes (Fig. 1).What is the most likely diagnosis? B) Stress-induced (takotsubo) cardiomyopathyFigure 1 shows sinus tachycardia with premature atrial contractions, new ST-segment elevations (STEs) in the inferior leads and in leads V2 through V6, and T-wave inversions throughout. Figure 2 shows the admission ECG.According to the Mayo Clinic criteria, the most common ECG changes associated with takotsubo cardiomyopathy (TTC) are STE and T-wave inversion. These changes are seen frequently in the precordial leads.1 Clinically, distinguishing TTC from acute coronary syndrome is challenging because of overlapping symptoms, elevated cardiac enzyme levels, and similar ECG changes. Certain ECG patterns indicate TTC rather than acute coronary syndrome, including the absence of ST-segment depression in the reciprocal leads; diffuse STEs extending beyond the territory of a single coronary artery; and STE in lead aVR with STE in the inferior, anterior, or anteroseptal leads.2Patients with suspected TTC may have known coronary artery disease (CAD) or associated risk factors; therefore, STEMI must be ruled out when STE is seen on an ECG.3 If angiograms reveal no fixed obstructive CAD, acetylcholine testing may be considered, because spasm-induced coronary obstruction has been proposed as the mechanism underlying TTC, with atherosclerotic CAD providing a protective “stenting” effect.4 Pulmonary embolism may trigger sinus tachycardia and T-wave inversions, but without STE or pulmonary edema. Wellens syndrome can cause isolated deep T-wave inversions in leads V1 through V3, but it cannot explain inferior-lead STE and T-wave changes.The pathophysiology of TTC involves transient stunning and reversible left ventricular (LV) systolic dysfunction after physiologic or emotional stress. Fewer than 20 cases of TTC have been reported as complications of acute pancreatitis. Of note, pancreatitis itself can cause STE, typically in the inferior leads.5 In our patient's case, an echocardiogram and left ventriculogram revealed severe apical hypokinesis and an LV ejection fraction of 40%; however, a coronary angiogram did not reveal obstructive CAD, so the diagnosis was TTC. Two months later, he had normal LV ejection function, consistent with expected recovery timelines.

Prevalence and impact of takotsubo syndrome in hospitalizations for acute ischemic stroke

Takotsubo syndrome (TTS) is characterized by acute and reversible left ventricular dysfunction with apical ballooning arising during acute stress situations. Acute ischemic stroke (AIS) is one of the known triggers of TTS; however, the impact of TTS on in-hospital outcomes of AIS remains unexplored. We utilized data from the National Inpatient Sample (2007–2014) to identify admissions for AIS with TTS and evaluated the temporal trends, baseline characteristics, in-hospital complications, length of stay, and all-cause mortality. Survey multivariable logistic regression was used to compute adjusted odds ratios (OR) and 95% confidence intervals (CI). An estimated 2242 (0.4%) TTS cases were identified among AIS hospitalizations (N = 4,392,471). The frequency of TTS was higher in elderly, white, and female patients. After adjustment for confounders, TTS incidence in AIS was associated with higher odds of in-hospital complications including cardiogenic shock (OR 8.84, CI 4.07–19.17, P < 0.001), cardiac arrest (OR 3.17, CI 1.57–6.42, P = 0.001), and venous thromboembolism (OR 1.68, CI 1.14–2.47, P = 0.008). Moreover, AIS hospitalizations with TTS showed higher odds of developing respiratory failure (OR 3.13, CI 2.42–4.05, P < 0.001) and requiring mechanical ventilation/intubation (OR 4.09, CI 3.14–5.32, P < 0.001) compared to the non-TTS cohort. The AIS-TTS cohort had a longer length of stay (8.59 vs 5.22 days), and their mortality rate was twice (10.2% vs 5.1%; P < 0.001) that of those without TTS. In conclusion, the prevalence of TTS in AIS remained ∼20 times higher than in the general inpatient population and predisposed AIS patients to worse inpatient outcomes. Further studies are needed to evaluate the impact of TTS on long-term outcomes in AIS.

Cognitive disorders in takotsubo syndrome: incidence, short and long-term outcome. Results from a prospective multi-center registry

Abstract Background Takotsubo syndrome (TTS) is an acute and reversible left ventricular dysfunction, whose pathophysiological mechanisms are not completely known. There are evidence suggesting a possible link between neurological disease and TTS. Aim of the study was to evaluate incidence and prognostic value of cognitive neurological disorders among TTS patients. Methods 379 consecutive patients were enrolled in a prospective multicenter registry. History, clinical features, echocardiographic parameters, in-hospital complications and long-term follow up events of all patients were recorded. Cognitive neurological disorders included Alzheimer disease, old age dementia and cognitive impairment for other causes. Results Prevalence of cognitive neurological disorders among TTS patients was 5.5% (num=21). Among this subset of patients 48% (num=10) had Alzheimer syndrome, 24% (num=5) old age dementia and 28% (num=6) cognitive impairment for other causes. Compared to the control group, these patients were older (81±5 vs 71±12, p=0.01) and predominantly men (24% vs 9%, p=0.01). No differences in term of cardiovascular risk factors and left ventricular ejection fraction at admission and discharge were found among the two groups. TTS patients with cognitive neurological disorders experienced higher rate of in-hospital complications (62% vs 28% p=0.01), that were mainly driven by higher rate of pulmonary edema (14% vs 9% p=0.01), cardiogenic shock (29% vs 8%, p=0.01), death (24% vs 4% p=0.01), ischemic stroke (10% vs 4% p=0.01) and left ventricular thrombi (10% vs 3%, p=0.01). At long term follow up patients with cognitive neurological disorders when compared to those without, experienced higher rate of mayor cardiovascular events (48% vs 16%, p=0.01), cardiovascular re-hospitalization (14% vs 10%, p=0.01) and death (43% vs 9%, p=0.01). Conclusion TTS patients with cognitive neurological disorders had an increased risk of in and out of hospital mayor cardiac adverse events and mortality at short and long-term follow-up. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Ospedali Riuniti di Foggia-Università di Foggia