Cerebrovascular events in left ventricular hypertrabeculation/noncompaction with and without myopathy

Finsterer, Josef; Stöllberger, Claudia; Mölzer, Günther; Winkler-Dworak, Maria; Blazek, Gerhard

doi:10.1016/j.ijcard.2007.08.089

Cited by 27 publications

(24 citation statements)

References 22 publications

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“…However, the question whether the risk of stroke is generally increased in LVHT patients is still unsolved. Some studies found no increased risk of stroke in LVHT patients [92,93], whereas others, particularly case reports or small case series, found an increased stroke risk [34, [94][95][96]. In a retrospective study on 229 patients with LVHT but without atrial fibrillation or flutter, stroke developed only in four patients during a mean follow-up of 7.3 years [92].…”

Section: Cardioembolismmentioning

confidence: 99%

Left ventricular non-compaction and its cardiac and neurologic implications

Finsterer

2010

Heart Fail Rev

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Left ventricular non-compaction, also known as left ventricular hypertrabeculation (LVHT), is a morphological abnormality of the left ventricular myocardium, characterised by a meshwork of myocardial strings, interlacing, and orderless in arrangement. LVHT is most frequently located in the apex and the lateral wall and may occur with or without other congenital or acquired cardiac abnormalities. LVHT is believed to be congenital in the majority of the cases but may develop during life in single cases (acquired LVHT). Congenital LVHT is believed to result from defective late-stage embryonic development of the myocardial architecture. The pathogenesis of acquired LVHT remains speculative. LVHT is most frequently found on transthoracic echocardiography and cardiac MRI but may be visualised also with other imaging techniques. In the majority of the cases, LVHT is associated with hereditary cardiac, neuromuscular, non-cardiac/non-muscle disease, or chromosomal aberrations. In the majority of the cases, LVHT is complicated by ventricular arrhythmias, systolic dysfunction, cardiac embolism, or sudden cardiac death. LVHT per se does not require a specific treatment. Only in case of complications, such as ventricular arrhythmias, cardioembolism, or systolic dysfunction, adequate therapy is indicated. Though initially assessed as poor, the prognosis of LVHT has meanwhile improved, most likely due to the increased awareness for the abnormality and the timely administration of adequate therapy.

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Section: Cardioembolismmentioning

confidence: 99%

Left ventricular non-compaction and its cardiac and neurologic implications

Finsterer

2010

Heart Fail Rev

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“…7 How do the authors explain the low rate of LVHT patients with atrial fibrillation compared to previous reports? 8 Since LVHT may affect several members of the same family, it would be of interest to know if any of the investigated patients were related, or if other family members were routinely investigated for familial LVHT?…”

Section: To the Editormentioning

confidence: 99%

Even Isolated Left Ventricular Hypertrabeculation May Indicate Multisystem Disease

Finsterer

Stöllberger

2010

Circ J

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“…Some studies found no increased frequency of stroke in LVHT patients [19,20,21], whereas others, particularly case reports, indicated an increased risk of developing a stroke (table 3) [22,23,24,25]. In a retrospective study of 229 patients with LVHT, of which those with AFI/AFL were excluded, only 4 patients had developed ischemic stroke during a mean follow-up of 7.3 years [19].…”

Section: Causes Of Stroke In Myopathiesmentioning

confidence: 99%

“…Though OAC have been frequently proposed for patients with LVHT [26], these recommendations rely only on single case reports or small case series. According to our own experience, there is no general indication for OAC in LVHT patients as long as classical indications for OAC therapy are absent [14,20]. …”

Section: Causes Of Stroke In Myopathiesmentioning

confidence: 99%

Stroke in Myopathies

Finsterer

Stöllberger

2009

Cerebrovasc Dis

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Objectives: Only few data are available about the risk of myopathy patients experiencing a cerebral stroke. Aims: To review the current knowledge about the frequency, pathogenesis, and outcome of stroke in primary/secondary myopathies. Methods: Literature review of all human studies dealing with stroke in primary/secondary myopathies. Results: Stroke in myopathies may be either ischemic, metabolic, or cryptogenic. Ischemic stroke may be further classified as cardioembolic, angiopathic, hemodynamic, or thrombophilic. Cardioembolic stroke occurs if there is cardiac involvement in the form of atrial fibrillation/flutter, dilated cardiomyopathy, or non-compaction. Angiopathic stroke occurs if there is atherosclerosis (frequently associated with mitochondrial disorders (MIDs), vasculitis, or dissection in inflammatory myopathies) or MIDs. Thrombophilic stroke may occur in poly-/dermatomyositis if there is additional anti-phospholipid syndrome. Metabolic stroke usually manifests as stroke-like episode and is a distinct feature of various MIDs, particularly MELAS syndrome. The clinical manifestations are due to a vasogenic edema, showing up as hyperintensity on T₂, DWI, and apparent diffusion coefficient mapping. Differentiation between ischemic and metabolic stroke is essential in terms of diagnosis, therapy, and prognosis. Conclusions: Ischemic stroke due to cardioembolism, arteriopathy, or thrombophilia are rare events in myopathies, but metabolic stroke is a frequent feature of MIDs, with distinct diagnostic and therapeutic implications.

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Cerebrovascular events in left ventricular hypertrabeculation/noncompaction with and without myopathy

Cited by 27 publications

References 22 publications

Left ventricular non-compaction and its cardiac and neurologic implications

Left ventricular non-compaction and its cardiac and neurologic implications

Even Isolated Left Ventricular Hypertrabeculation May Indicate Multisystem Disease

Stroke in Myopathies

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