From the Guidelines
Cardiomyopathy in cerebral vascular accident (CVA) or stroke is primarily caused by a catecholamine-mediated process, leading to stress-induced cardiomyopathy, also known as Takotsubo cardiomyopathy.
Mechanism of Cardiomyopathy
- The mechanism underlying stress-induced cardiomyopathy is not well understood, but evidence supports an adrenergically mediated process 1.
- Catecholamine surges are an evolutionary response to stress and danger, and supraphysiological elevations of plasma catecholamines have been demonstrated in stress cardiomyopathy 1.
- The ventricular apex has relatively sparse sympathetic innervation, but it is more responsive to sympathetic stimuli due to increased β2-adrenergic receptor density 1.
- Other theories include microvascular vasospasm and impaired fatty acid metabolism 1.
Clinical Presentation
- Stress-induced cardiomyopathy presents similarly to acute myocardial infarction with chest pain, ST-segment elevation on ECG, and elevated cardiac enzymes 1.
- It accounts for 2% of myocardial infarction with nonobstructive coronary arteries (MINOCA) 1.
Diagnosis and Treatment
- Diagnosis is made based on the Mayo Clinic or InterTAK diagnostic criteria 1.
- Treatment involves managing the underlying cause of the stress-induced cardiomyopathy, and may include anticoagulation therapy to prevent cardioembolic events 1.
- However, the use of warfarin in patients with cardiac failure or reduced LV EF is still a topic of controversy, and aspirin may be used as an alternative 1.
From the Research
Mechanism of Cardiomyopathy in CVA or Stroke
The mechanism of cardiomyopathy in cerebral vascular accident (CVA) or stroke is complex and involves multiple pathways. Some of the key mechanisms include:
- Catecholamine-induced cardiotoxicity, which is a critical element in the pathophysiology of stroke-induced heart injury 2
- Damage from gut dysbiosis, immune and systematic inflammatory responses, microvesicle- and microRNA-mediated vascular injury, and damage from a surge of catecholamines 2
- Myocardial ischemia, calcium (Ca2+) overload, oxidative stress, and mitochondrial dysfunction, which are all caused by the primary catecholamines involved in this pathophysiological response, including norepinephrine (NE) and epinephrine 2
- Takotsubo cardiomyopathy, which has been described as a consequence of stroke or a cardioembolic source of stroke, and is characterized by transient left ventricular apical ballooning 3, 4
Role of Catecholamines
Catecholamines, such as norepinephrine (NE) and epinephrine, play a crucial role in the mechanism of cardiomyopathy in CVA or stroke. These neurotransmitters connect the nervous system with the heart, leading to cardiac damage via:
- Myocardial ischemia
- Calcium (Ca2+) overload
- Oxidative stress
- Mitochondrial dysfunction 2
Clinical Characteristics
The clinical characteristics of patients who experience cardiomyopathy in CVA or stroke include:
- Female sex
- Insular damage
- Vertebrobasilar stroke
- Abnormal findings on electrocardiographic monitoring
- Elevated plasma brain natriuretic peptide levels 4