Related Experiment Video
Updated: Jun 19, 2026
04:48
Noninvasive Determination of Vortex Formation Time Using Transesophageal Echocardiography During Cardiac Surgery
Published on: November 28, 2018
8.2K
Left ventricular non-compaction as a potential source for cryptogenic ischemic stroke in the young: A case-control
Pauli Pöyhönen1, Jouni Kuusisto1, Vesa Järvinen2
1Heart and Lung Center, Helsinki University Hospital and Helsinki University, Helsinki, Finland.
Plos One
|August 16, 2020
Summary
Left ventricular non-compaction is linked to increased risk of cryptogenic ischemic stroke in young adults. This finding holds true even without patent foramen ovale or cardiomyopathy, suggesting a novel stroke etiology.
Area of Science:
- Cardiology
- Neurology
- Medical Imaging
Background:
- Cryptogenic ischemic strokes affect up to 50% of young adults.
- Patent foramen ovale (PFO) is a common but low-risk source of embolism.
- Left ventricular (LV) non-compaction may cause stroke due to sluggish blood flow.
Purpose of the Study:
- Investigate LV non-compaction as a source of cryptogenic stroke in young adults.
- Assess the association between LV non-compaction and stroke etiology.
- Determine if LV non-compaction is an independent risk factor for stroke.
Main Methods:
- Prospective, multicenter case-control study (SECRETO; NCT01934725).
- 30 young stroke cases (18-49 years) and 30 controls underwent cardiac magnetic resonance (CMR).
- Transcranial Doppler (TCD) bubble test evaluated right-to-left shunt (RLS).
Main Results:
- No significant differences in LV volumes, mass, or systolic function between groups.
- LV non-compaction (mass and volume) was significantly higher in stroke cases.
- Increased LV non-compaction and RLS were independently associated with cryptogenic stroke.
Conclusions:
- LV non-compaction is a significant risk factor for cryptogenic ischemic stroke in young adults.
- This association is independent of RLS and the absence of cardiomyopathy.
- LV non-compaction represents a potential embolic source in young stroke patients.
Related Concept Videos
01:17Ischemic Heart Disease: Overview
Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
01:26Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
01:15Ischemic Stroke l: Introduction
Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
01:15Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
01:29Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
01:26Transient Ischemic Attack l: Introduction
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...