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Coronary artery spasm (CAS), or Prinzmetal angina, is a recognised cause of myocardial ischaemia in non-obstructed coronary arteries which typically presents with anginal chestpain. The patient presented with recurrent palpitations and pre-syncope, with no chestpain.
Written by Colin Jenkins and Nhu-Nguyen Le with edits by Willy Frick and by Smith A 46-year-old male presented to the emergency department with 2 days of heavy substernal chestpain and nausea. The patient continued having chestpain. There are three mechanisms of arrhythmia: automatic, re-entry, and triggered.
Arrhythmias (Abnormal Heart Rhythms) Stress hormones can disrupt the signals that regulate your heartbeat, leading to arrhythmias – abnormal heart rhythms that cause your heart to beat too fast, too slow, or irregularly.
They also documented "Reproducible chest tenderness." Remember, reproducible chest tenderness should not reassure you in patients with high pre-test probability of OMI. Thus, the patient does not (yet) get a formal diagnosis of MI and must be called unstable angina unless further troponins return above the 99th percentile.
Background On the one hand, the primary coronary slow flow phenomenon (CSFP) can cause recurrence of chestpain, prompting medical examinations and further healthcare costs, while on the other hand, it can lead to myocardial infarction, ventricular arrhythmia and sudden cardiac death.
Therefore this is " Transient ST Elevation Unstable Angina." As there was ruptured plaque, this is NOT Prinzmetal's angina. Here are many other cases of Unstable Angina , in spite of Eugene Braunwald's Requiem for Unstable Angina. So Unstable Angina still exists [even with high sensitivity (hs) troponins].
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chestpain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. BP was 160/100.
This should result in at least some positivity of QRS complexes as one moves toward the lateral chest leads. The finding of all negative QRS complexes in leads V3-thru- V6 therefore strongly suggests that the arrhythmia-associated impulse is not traveling over an AP ( Steurer et al — Clin. Cardiol 17:306-308, 1994 ).
Written by Willy Frick A man in his 60s with hypertension and prior stroke presented with three days of crushing chestpain. He reported intermittent chestpain for the last few months, but never lasting this long. The cardiology consultant notes that pain is "almost resolved." There is active infarction.
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