What is the mechanism of cardiomyopathy in cerebral vascular accident (CVA) or stroke?

From the Guidelines

Cardiomyopathy in cerebral vascular accident (CVA) or stroke is primarily caused by stress-induced cardiomyopathy, also known as Takotsubo cardiomyopathy, which is attributed to catecholamine release, possibly following a stressful event.

Mechanism of Cardiomyopathy

• The mechanisms underlying stress-induced cardiomyopathy are 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.
• 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.
• LVOT obstruction, arrhythmia, shock, ventricular rupture, thrombus, and death may also be seen 1.

Diagnosis

• Diagnosis is made based on the Mayo Clinic or InterTAK diagnostic criteria 1.
• ECG, serological biomarkers, and imaging tests are used to evaluate patients with suspected cardiomyopathy 1.

Relationship between Cardiomyopathy and Stroke

• Cardiomyopathies, including diseases of the atria and ventricles, can increase the risk of stroke, even in the absence of atrial fibrillation 1.
• Impaired left ventricular systolic function can create a condition of relative stasis within the left ventricle, activating coagulation processes and increasing the risk of thromboembolic events 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 caused by primary catecholamines such as norepinephrine (NE) and epinephrine 2
• Stress-induced cardiomyopathy (Takotsubo cardiomyopathy), which may be caused by heat stroke and is characterized by an increase in serum catecholamine levels 3

Role of Catecholamines

Catecholamines, such as norepinephrine and epinephrine, play a key role in the mechanism of cardiomyopathy in CVA or stroke. They can cause:

• Myocardial stunning in Takotsubo cardiomyopathy and some cases of cerebral ischemia 4
• Cardiac damage via myocardial ischemia, calcium (Ca2+) overload, oxidative stress, and mitochondrial dysfunction 2
• Increase in serum catecholamine levels, which can lead to stress-induced cardiomyopathy 3

Classification of Cardiomyopathies

Cardiomyopathies can be classified into primary, secondary, and those in which cardiomyopathy is the first/predominant manifestation of a neuromuscular disorder 5. Secondary cardiomyopathies may be caused by neurological disorders, and management of these conditions requires early cardiologic investigations and close follow-ups 5.

Neurologic Complications of Cardiomyopathies

Cardiomyopathies can result in neurologic complications, including embolic stroke, which is associated with thrombus and depressed left ventricular ejection fractions 6. Anticoagulation can significantly reduce the incidence of thrombotic problems, and patent foramen ovale has created interest in those patients with cryptogenic strokes 6.