Wellens Syndrome Publications (227)
Wellens Syndrome Publications
Since myocardial infarction does not typically present with syncope, we explored the differential diagnoses for T-wave inversions, which include electrolyte abnormalities, medications, intracranial hemorrhage, pulmonary embolism, and other cardiac diseases that were ruled out in our patient. We also explored the pathophysiology leading to syncope in the setting of acute myocardial infarction including arrhythmias and exaggerated neurally mediated response. Our patient received two drug-eluting stents to the LAD artery and was started on dual antiplatelet therapy, beta-blockers, and an angiotensin-converting enzyme inhibitor.
Therefore, even subtle signs of an anterior wall infarction diagnosed by the ECG which lead to suspicion of complete occlusion of a coronary artery should be known and diagnosed by all physicians who may have contact with these types of patients. The ECG variations presented in this article can be used as a sample for medical personnel who are not familiar with these changes and do not routinely interpret ECGs.
Here, we report a case of an overweight man with 35 pack-year of smoking history who presented to Easton Hospital with intermittent pressing chest pain of 5/6 times within 10 day-period and was found to have type A Wellens' sign, which was biphasic T-waves in precordial leads V2 and V3 during pain-free period with no cardiac enzymes elevation. He was given therapeutic lovenox and subsequently underwent coronary angioplasty and had 95-99% occlusion in proximal LAD artery. The unique feature of our case was that Wellens' type B EKG changes were seen after reduction of stenosis with LAD artery stent, which was likely explained by the reperfusion of the ischemic myocardium. Therefore, it is important for physicians to recognize EKG features of Wellens' syndrome in order to take appropriate therapy to reducing mortality and morbidity form impending MI.
Intravenous Diltiazem was administered following which there was resolution of atrial fibrillation as well as his chest pain. Troponin T and CPK-MB were minimally elevated at 0.05ng/ml (0.0-0.03ng/ml) and 8.6ng/ml (0.0-7.0ng/ml) respectively. A repeat EKG obtained after symptom resolution showed biphasic T wave inversions in V2 and V3 which prompted an emergent coronary angiogram that revealed 90% occlusion of the proximal LAD. The immediate recognition of Wellens' pattern lead to emergent coronary revascularization and prevention of acute myocardial infarction in our patient. Clinicians should be aware of this syndrome so that prompt invasive therapy can be done to avoid evolution into MI and subsequent left ventricular dysfunction.
We included 447 probands belonging to families with a diagnostic type 1 electrocardiogram Brugada pattern. The database was divided into 2 periods: the first period identified patients who were part of the initial cohort that became the consensus document on BrS in 2002 (early group); the second period reflected patients first diagnosed from 2003 to January 2014 (latter group).
There were 165 probands in the early group and 282 in the latter group. Aborted sudden death as the first manifestation of the disease occurred in 12.1% of the early group versus 4.6% of the latter group (p = 0.005). Inducibility during programmed electrical stimulation was achieved in 34.4% and 19.2% of patients, respectively (p < 0.001). A spontaneous type 1 electrocardiogram pattern at diagnosis was present in 50.3% early versus 26.2% latter patients (p = 0.0002). Early group patients had a higher probability of a recurrent arrhythmia during follow-up (19%) than those of the latter group (5%) (p = 0.007). The clinical suspicion and use of a sodium-channel blocker to unmask BrS has allowed earlier diagnoses in many patients.
Since being first described, the presentation of BrS has changed. There has been a decrease in aborted sudden cardiac death as the first manifestation of the disease among patients who were more recently diagnosed. These variations in initial presentation have important clinical consequences. In this setting, the value of inducibility to stratify individuals with BrS has changed.
Review of ECGs from patients with ST elevation MI of the left circumflex or right coronary artery with post-procedure thrombolysis in MI (TIMI) flow >0 between 2007 and 2009. Blinded experts reviewed admission ECGs to determine the presence of PMI and measure TWa before and after reperfusion. Maximum TWa in V2 and V3 and the difference between maximum and admission V2 and V3 TWa were compared between those with and without PMI.
Of 72 patients, 48 had PMI. Values expressed are medians and IQRs. Maximum TWa after reperfusion was greater in PMI than in non-PMI in V2 (5.00 mm (3.5 to 8.25) vs 3.9 mm (2.75 to 5.5), p=0.04), but not in V3 (4.0 mm (2 to 5.5) vs 3.0 mm (1.75 to 4), p=0.09). The increase in TWa in V2 and V3 after reperfusion was greater in PMI compared with non-PMI: (V2, 3.4 mm (2 to 5.25) vs 1.25 mm (-0.25 to 2), p=0.0005; V3, 2 mm (-0.5 to 3.25) vs 0.25 mm (-1 to 1.75), p=0.03).
Reperfusion of the posterior wall results in higher right precordial TWa, and an even greater increase in TWa, as measured in leads V2 and V3. This observation has important implications for emergency physicians to accurately identify recent posterior infarction in patients who may be symptom free on presentation but at risk of reocclusion.
Emergency coronary angiography showed severe stenosis (99%) in proximal LAD.