scholarly journals Cardio-oncology: what you need to know now for clinical practice and echocardiography

2017 ◽  
Vol 4 (1) ◽  
pp. R33-R41 ◽  
Author(s):  
Carolyn M Larsen ◽  
Sharon L Mulvagh
Keyword(s):  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Chemotherapeutic Agents ◽  
Left Ventricular ◽  
Baseline Assessment ◽  
Oncology Patients ◽  
Cardiovascular Morbidity And Mortality ◽  
Increased Risk

Cardio-oncology is a rapidly growing field aimed at minimizing the effects of cardiovascular morbidity and mortality in cancer survivors. To meet this aim, patients are assessed at baseline to define their risk of cardiotoxicity and then followed closely during and after chemotherapy to assess for early signs or symptoms of cardiovascular disease. Cardiac imaging, and in particular, transthoracic echocardiography, plays an essential role in the baseline assessment and serial follow-up of cardio-oncology patients. The objectives of this paper are to review the mechanisms of cardiotoxicity of several common chemotherapeutic agents associated with an increased risk for left ventricular systolic dysfunction and to outline recommendations regarding the baseline assessment and serial follow-up of cardio-oncology patients with a focus on the role of echocardiography.

P1868Risk of arrhythmias after myocardial infarction in patients with left ventricular systolic dysfunction according to mode of revascularization: a CARISMA substudy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Thomsen ◽  
S Pedersen ◽  
P K Jacobsen ◽  
H V Huikuri ◽  
P E Bloch Thomsen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Loop Recorder ◽  
Ventricular Ejection Fraction ◽  
New Onset

Abstract Introduction The CARISMA trial was the first study to use continuous monitoring for documentation of long-term arrhythmias in post-infarction patients with left ventricular dysfunction. During the study duration (2000–2005), primary PCI (pPCI) as treatment of acute myocardial infarction was introduced approximately midway (2002) on the enrolling centres. Purpose The aim of this study was to describe the influence of mode of revascularization after myocardial infarction (AMI) on long-term risk of risk of new onset atrial fibrillation, ventricular tachyarrhythmias and brady arrhythmias. Methods The study is a sub-study on the CARISMA study population that consisted of patients with AMI and left ventricular ejection fraction ≤40%, which received an implantable loop recorder and was followed for 2 years. After exclusion of 15 patients who refused device implantation and 26 with pre-existing arrhythmias, 268 of the 312 patients were included. Choice of revascularization was made by the treating team independently of the trial and was retrospectively divided into primary percutaneous intervention (pPCI), subacute PCI (24 hours to 2 weeks after AMI), primary thrombolysis or no revascularization. Endpoints were new-onset of arrhythmias and major cardiovascular events (MACE). The Kaplan-Meier (figure 1) and Mantel-Byar methods were used for time to first event risk analysis. Results A total of 77 patients received no revascularization, whereas 49 received thrombolysis only and 142 received PCI. At two-years follow up patients treated with any PCI had a significant lower risk (0.40, n=63) of any arrhythmia compared to patients treated with trombolysis (0.60, n=30) or no revascularization (0.68, n=16) (p<0.001, unadjusted) (figure 1). Risk of MACE was significant higher in patients with any arrhythmia (0.25, n=76) compared to no arrhythmia (0.11, n=93) at two years follow-up (p=0.004, unadjusted). Figure 1 Conclusion(s) The long-term risk of new onset arrhythmias after AMI was significantly lower in patients treated with any PCI compared to patients not revascularized or treated with thrombolysis. Risk of MACE was significantly higher in patients with new onset arrhythmias compared to patients with no arrhythmias.

scholarly journals Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

2020 ◽  
Vol 21 (3) ◽  
pp. 807 ◽  
Author(s):  
Iwona Świątkiewicz ◽  
Przemysław Magielski ◽  
Jacek Kubica ◽  
Adena Zadourian ◽  
Anthony N. DeMaria ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Multivariable Analysis ◽  
High Sensitivity ◽  
Left Ventricular ◽  
St Segment Elevation ◽  
Reactive Protein

Acute ST-segment elevation myocardial infarction (STEMI) activates inflammation that can contribute to left ventricular systolic dysfunction (LVSD) and heart failure (HF). The objective of this study was to examine whether high-sensitivity C-reactive protein (CRP) concentration is predictive of long-term post-infarct LVSD and HF. In 204 patients with a first STEMI, CRP was measured at hospital admission, 24 h (CRP24), discharge (CRPDC), and 1 month after discharge (CRP1M). LVSD at 6 months after discharge (LVSD6M) and hospitalization for HF in long-term multi-year follow-up were prospectively evaluated. LVSD6M occurred in 17.6% of patients. HF hospitalization within a median follow-up of 5.6 years occurred in 45.7% of patients with LVSD6M vs. 4.9% without LVSD6M (p < 0.0001). Compared to patients without LVSD6M, the patients with LVSD6M had higher CRP24 and CRPDC and persistent CRP1M ≥ 2 mg/L. CRP levels were also higher in patients in whom LVSD persisted at 6 months (51% of all patients who had LVSD at discharge upon index STEMI) vs. patients in whom LVSD resolved. In multivariable analysis, CRP24 ≥ 19.67 mg/L improved the prediction of LVSD6M with an increased odds ratio of 1.47 (p < 0.01). Patients with LVSD6M who developed HF had the highest CRP during index STEMI. Elevated CRP concentration during STEMI can serve as a synergistic marker for risk of long-term LVSD and HF.

scholarly journals Diabetic cardiomyopathy: acute and reversible left ventricular systolic dysfunction due to cardiotoxicity of hyperglycaemic hyperosmolar state—a case report†

2019 ◽  
Vol 3 (2) ◽  
Author(s):  
Umut Kocabaş ◽  
Özgür Yılmaz ◽  
Volkan Kurtoğlu
Keyword(s):  
Blood Glucose ◽  
Diabetic Cardiomyopathy ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Blood Glucose Control ◽  
Left Ventricular ◽  
Pathophysiological Mechanism ◽  
Ventricular Systolic Dysfunction ◽  
Arterial Blood

Abstract Background Diabetic cardiomyopathy (DC) is defined as a ventricular diastolic and/or systolic dysfunction, which is directly related to diabetes mellitus (DM) in the absence of coronary artery disease, valvular, congenital or hypertensive heart disease, and alcoholism. In this report, we present an unusual case of a patient with DC and reversible, acute left ventricular systolic dysfunction due to cardiotoxicity of hyperosmolar hyperglycaemic state (HHS). Case summary A 20-year-old male patient presented with weakness and polyuria. Physical examination and electrocardiogram were normal. Laboratory results and arterial blood gas analysis were consistent with HHS. Baseline echocardiography showed global left ventricular hypokinesis with an ejection fraction (EF) of 36%. The patient’s clinical condition improved after blood glucose level normalization and echocardiography revealed progressive improvement in the left ventricular systolic function with an EF of 54% at the 5-day follow-up and an EF of 69% at the 15-day follow-up. Discussion Uncontrolled DM and hyperglycaemic crisis may result in cardiotoxicity, acute left ventricular systolic dysfunction, and DC. The pathophysiological mechanism of this phenomenon is still unclear. Blood glucose control is the most important strategy for the prevention of DC.

scholarly journals P1441 Predictors of systemic embolisms in a large cohort of left ventricular noncompaction patients

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
G Casas ◽  
G Oristrell ◽  
J Limeres ◽  
R Barriales ◽  
J R Gimeno ◽  
...  
Keyword(s):  
Risk Factors ◽  
Atrial Fibrillation ◽  
Oral Anticoagulation ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Severe Phenotype ◽  
Ventricular Noncompaction ◽  
Increased Risk

Abstract BACKGROUND Left ventricular noncompaction (LVNC) is associated with an increased risk of systemic embolisms (SE). However, incidence and risk factors are not well established. PURPOSE To evaluate the rate of SE in LVNC and describe risk factors. METHODS LNVC patients were included in a multicentric registry. Those with SE were considered for the analysis. RESULTS 514 patients with LVNC from 10 Spanish centres were recruited from 2000 to 2018. During a median follow-up of 4.2 years (IQR 1.9-7.1), 23 patients (4.5%) had a SE. Patients with SE (Table 1) were older at diagnosis, with no differences in gender and had similar cardiovascular risk factors. They were more frequently under oral anticoagulation (OAC). Besides, they had a more reduced LVEF, and more dilated LV and left atrium (LA). Late gadolinium enhancement (LGE) was more frequent, altogether suggesting a more severe phenotype. Patients with SE had non-significantly higher rates of hospitalization for heart failure (33% Vs 24%, p = 0.31) and atrial fibrillation (35% Vs 19%, p = 0.10). In multivariate analysis, only LA diameter was an independent predictor of SE (OR 1.04, p = 0.04). A LA diameter &gt; 45 mm had an independent 3 fold increased risk of SE (OR 3.04, p = 0.02) (Image 1). CONCLUSIONS LVNC carries a moderate mid-term risk of SE, which appears to be irrespective of atrial fibrillation and associated with age, LV dilatation and systolic dysfunction and mainly LA dilatation. This subgroup of patients should be considered for oral anticoagulation in primary prevention. Table 1 Systemic embolisms (n = 23) No systemic embolisms (n = 491) p Men, n (%) 15 (65) 289 (56) 0.52 Median age at diagnosis (IQR) - yr 60 (48-76) 48 (30-64) 0.02 Median follow up (IQR) - yr 5.9 (3.1-7.8) 4.2 (1.8-7.1) 0.18 OAC, n (%) 19 (83) 118 (24) 0.01 LVEF (SD) - % 37 (15) 48 (17) 0.01 LVEDD (SD) - mm 58 (11) 54 (10) 0.04 LA diameter (SD) - mm 46 (9) 39 (9) 0.01 Characteristics of patients with and without systemic embolisms Abstract P1441 Figure. Image 1

scholarly journals Trimetazidine modified release in treatment of patients with the serious course of chronic ischemic heart disease: from the theory to real clinical practice

2014 ◽  
Vol 5 (1) ◽  
pp. 56-62
Author(s):  
A. V Barsukov ◽  
D. V Glukhovskoy
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Modified Release ◽  
Ventricular Systolic Dysfunction ◽  
Chronic Ischemic Heart Disease

The paper considers modern conceptions about the role of citoprotective therapy in persons with ischemic heart disease. Special attention is given to the justification of Trimetazidine modified release (TMZ MV) application in patients with severe multi-vessel coronary lesions in conjunction with left ventricular systolic dysfunction. There described the clinical case with emphasis on possibility of inclusion in conservative treatment scheme of TMZ MB to poly morbid elderly patient with severe ischemic heart disease.

scholarly journals The role of central autonomic nervous system dysfunction in Takotsubo syndrome: a systematic review

2022 ◽  
Author(s):  
Vojtech Brazdil ◽  
Petr Kala ◽  
Martin Hudec ◽  
Martin Poloczek ◽  
Jan Kanovsky ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Nervous System ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Takotsubo Syndrome ◽  
Autonomic Nervous System Dysfunction ◽  
Benign Condition ◽  
As Stress

Abstract Introduction Takotsubo syndrome (TTS), also known as stress cardiomyopathy or “broken heart” syndrome, is a mysterious condition that often mimics an acute myocardial infarction. Both are characterized by left ventricular systolic dysfunction. However, this dysfunction is reversible in the majority of TTS patients. Purpose Recent studies surprisingly demonstrated that TTS, initially perceived as a benign condition, has a long-term prognosis akin to myocardial infarction. Therefore, the health consequences and societal impact of TTS are not trivial. The pathophysiological mechanisms of TTS are not yet completely understood. In the last decade, attention has been increasingly focused on the putative role of the central nervous system in the pathogenesis of TTS. Conclusion In this review, we aim to summarize the state of the art in the field of the brain–heart axis, regional structural and functional brain abnormalities, and connectivity aberrancies in TTS.

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