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BackgroundPlaque progression (PP) is critical between subclinical atherosclerosis and plaque rupture. Journal of the American Heart Association, Ahead of Print. Small dense lowdensity lipoprotein cholesterol (sdLDLC) is considered as the most atherogenic lipoprotein.
We used carotid ultrasounds to detect plaque at baseline and follow‐up in 2006 to 2009 (median follow‐up=5.5 We identified incident CVD events through 2020 with a median follow‐up of 18.5 had incident plaque (109/1104 plaque‐free participants with baseline and follow‐up ultrasounds), 11.0%
The incidence of no-reflow was higher in patients with attenuated plaque ≥5 mm in length as evaluated by intravascular ultrasound (IVUS).Objective:The The incidence of no-reflow was higher in patients with attenuated plaque ≥5 mm in length as evaluated by intravascular ultrasound (IVUS).Objective:The vs. 41.2%, p=0.043).Conclusion:In
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. Thus, intracoronary imaging modalities are crucial in this setting. From Gue at al.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. It is not rare.
If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. Here is my comment on MINOCA: "Non-obstructive coronary disease" does not necessarily imply "no plaque rupture with thrombus." They often cannot even be recognized as culprits, as fissured or ulcerated plaque.
EKG from triage: Here is his previous ECG: Normal ST Elevation Resident's interpretation: Reperfusion pattern/Wellens' with biphasic T waves in V2 and V3, and in comparison to an EKG in 2020 this is new. Bedside ultrasound with no apparent wall motion abnormalities, no pericardial effusion, no right heart strain.
24: Joint American College of Cardiology/Journal of the American College of Cardiology Late-Breaking Clinical Trials (Session 402) Saturday, April 6 9:30 – 10:30 a.m.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
On arrival, lung ultrasound confirmed pulmonary edema (B lines). Mild Plaque no angiographically significant obstructive coronary artery disease. There is STE and hyperacute T-waves in V2 and V3, with significant STE in I and aVL, and inferior reciprocal STD. This is proximal LAD Occlusion until proven otherwise.
To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this. She was treated medically for NonSTEMI, pending next day cath, which showed ulcerated plaque and a 60% thrombotic stenosis in the LAD distal to the first diagonal. She said: This is a tough one.
A bedside ultrasound should be done to assess volume and other etiologies of tachycardia, but if no cause of type 2 MI is found, the cath lab should be activated NOW. As an aside, the LCx OMI is a type 2 event, since it is due to supply-demand mismatch from thrombus, and not due to atherosclerotic plaque rupture or erosion).
Only after her troponin peaked at 500,000 ng/L did she get her angiogram, which showed a 100% left main occlusion due to ruptured plaque. Beware a negative Bedside ultrasound. She died before she could get a heart transplant. They just could not believe that a young woman could have an OMI. RBBB, LAFB, and STE in I, aVL, V2 and V3.
Provocative testing is very helpful for this Coronary Thrombus with lysis (one must do optical coherence tomography or at least intravascular ultrasound to find thes non-obstructive plaques that ruptured. These plaques will often not be recognized as "culprits", because no fissuring or ulcertaion is seen. Embolism with lysis.
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