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Left ventricular thrombus formation and cardiac insufficiency were evident on echocardiogram, while multiple acute or subacute cerebral infarctions were visible on brain magnetic resonance imaging. Here, we report a rare case of a 28-year-old female patient who presented with chest tightness and dizziness.
Previous medical interventions included a spectrum of procedures, including catheter-directed thrombectomy for popliteal artery aneurysms with thrombosis, vascular bypass grafting for cerebral-anterior communicating artery aneurysms and arch replacement and stent implantation for aortic dissecting aneurysms.
vs. 30.4%, p =0.07) and device related thrombosis (4.5% vs. 4.5%, p =0.96) on transesophageal echocardiogram did not differ. Both major (1.4% vs. 2.1%, p =0.72) and minor (27.8% vs. 19.4%, p =0.17) in-hospital complications were similar between the combined and control group, respectively.
It is important to recognize that coronary thrombosis is dynamic , with spontaneous opening and lysing of the thrombus in the infarct-related artery (we all have endogenous tPA and plasmin to lyse thrombi). There are those who think that an echo that is done after resolution of ischemia is sensitive for that previous ischemia.
Blunt cardiac injury my result in : 1) Acute myocardial rupture with tamponade 2) Valve rupture (tricuspid, aortic, mitral) 3) Coronary thrombosis or dissection (and thus Acute MI) from direct coronary blunt injury 4) Dysrhythmias of all kinds. She was discharged to home feeling just fine.
Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection. ng/mL by 4th generation and older assays.)
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.
The patient was thought to have low likelihood of ACS, and cardiology recommended repeat troponin, urine drug testing, and echocardiogram. Bedside echocardiogram showed hypokinesis of the mid to distal anterior wall and apex. Initial hscTnI was 10 ng/L (ref. <14). There was no recommendation for repeat ECG.
Category 1 : Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates. elevated BP), but rather directly correlated with coronary obstruction (due to plaque rupture and thrombosis) and, potentially, stymied TIMI flow. This results in Type I MI.
See this case: what do you think the echocardiogram shows in this case? Widespread ST-depression with reciprocal aVR ST-elevation can be cause by: Heart rate related: tachyarrhythmia (e.g., POCUS showed good LV-function and no pericardial effusion. The patient had mild but diffuse abdominal tenderness.
I think a good start would be a posterior EKG and a high quality contrast echocardiogram read by an expert. It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. His prior EF from an ECHO 6 months prior indicated 35% LVEF. What would you do in this scenario?
In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%). So indeed the QRS is approximately 200 ms. Comment: What is the normal QRS duration in LBBB?
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