Rationale: The typical symptoms of stress cardiomyopathy include sudden-onset chest pain and breathlessness or collapse as well as classical symptoms of cardiovascular disease; however, rare reports have described nervous system symptoms as the initial manifestation. Here, we report the case of a young man who presented with a large cerebral infarction as the main clinical symptom of stress cardiomyopathy to increase recognition of the disease.
Patient Concerns: A 28-year-old man was admitted to our hospital for sudden-onset weakness of the right limbs and unconsciousness for 1 day. Ten days prior, he began consuming copious amounts of alcohol (500 mL/day) secondary to reactive depression.
Diagnoses: Imaging revealed a left internal carotid artery occlusion as assessed by carotid artery ultrasonography. Brain magnetic resonance imaging/magnetic resonance angiography showed new large left cerebral infarction complicated by a reperfusion injury. Moreover, cardiac ultrasonography showed decreased motion of the left ventricular apex, a 3.7 cm mural thrombus in the ventricular apex. The results of coronary and renal artery angiography did not reveal any significant epicardial coronary disease with thrombolysis in the myocardial infarction grade 3 in any of the coronary arteries.
Interventions: The patient was administered antiplatelet, anticoagulation, antihypertension, antibiotic, and neurotrophic therapies.
Outcomes: The symptoms of cerebral infarction improved significantly after 12 days of admission. Cardiac ultrasonography showed that the wall movement of the left ventricular apex had recovered fully and the mural thrombus resolved completely.
Lessons: Patients with stress cardiomyopathy exhibit various clinical manifestations and characteristics. On the basis of our in-depth understanding of stress cardiomyopathy, clinicians should diagnose early and develop reasonable and effective therapies to prevent the harmful effects of related complications.
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http://dx.doi.org/10.1097/MD.0000000000010804 | DOI Listing |
Int J Mol Sci
December 2024
Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Atrial fibrosis is a hallmark of atrial cardiomyopathy and plays a pivotal role in the pathogenesis of atrial fibrillation (AF), contributing to its onset and progression. The mechanisms underlying atrial fibrosis are multifaceted, involving stretch-induced fibroblast activation, oxidative stress, inflammation, and coagulation pathways. Variations in fibrosis types-reactive and replacement fibrosis-are influenced by patient-specific factors such as age, sex, and comorbidities, complicating therapeutic approaches.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Clinic of Nuclear Medicine Central University Emergency Military Hospital "Dr Carol Davila", 10825 Bucharest, Romania.
Amyloidosis is a rare pathology characterized by protein deposits in various organs and tissues. Cardiac amyloidosis (CA) can be caused by various protein deposits, but transthyretin amyloidosis (ATTR) and immunoglobulin light chain (AL) are the most frequent pathologies. Protein misfolding can be induced by several factors such as oxidative stress, genetic mutations, aging, chronic inflammation, and neoplastic disorders.
View Article and Find Full Text PDFPlants (Basel)
December 2024
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur 56000, Malaysia.
Diabetic cardiomyopathy is a significant and severe complication of diabetes that affects a large portion of the global population, with its prevalence continuing to rise. Secondary metabolites, including quercetin, have shown promising effects in mitigating the progression of diabetic cardiomyopathy by targeting multiple pathological mechanisms, including impaired insulin signaling, glucotoxicity, lipotoxicity, oxidative stress, inflammation, fibrosis, apoptosis, autophagy, mitochondrial dysfunction, cardiac stiffness, and disrupted calcium handling. Addressing these mechanisms is crucial to prevent left ventricular diastolic and systolic dysfunction in advanced stages of diabetic heart disease.
View Article and Find Full Text PDFLife Sci
January 2025
Department of Cardiology, Cardiac Arrhythmia Center, Affiliated Hospital of Nantong University, Nantong 226001, China. Electronic address:
Doxorubicin (DOX), a chemotherapeutic agent utilized in the management of cancer, provokes cardiotoxicity although effective remedy is lacking. Given that DOX provokes oxidative stress and cell death in cardiomyocytes, this study evaluated the possible involvement of cuproptosis, a newly identified form of cell death, in DOX-instigated cardiac remodeling and contractile dysfunction, alongside the impact of the heavy metal scavenger metallothionein (MT) on DOX cardiomyopathy. Cardiac-specific MT transgenic and wild-type (WT) mice were treated with DOX (5 mg/kg/wk.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA; Institute of Engineering Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Sanford Consortium for Regenerative Medicine, La Jolla, CA 92093, USA. Electronic address:
Vinculin (VCL) is a key adapter protein located in force-bearing costamere complexes, which mechanically couples the sarcomere to the ECM. Heterozygous vinculin frameshift genetic variants can contribute to cardiomyopathy when external stress is applied, but the mechanosensitive pathways underpinning VCL haploinsufficiency remain elusive. Here, we show that in response to extracellular matrix stiffening, heterozygous loss of VCL disrupts force-mediated costamere protein recruitment, thereby impairing cardiomyocyte contractility and sarcomere organization.
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