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Mohan Gamesh
Introduction
Preinfarction stage of coronary artery disease
1982 Wellens et al. published the clinical and ECG criteria of a subgroup of patients with myocardial
ischemia (Wellens syndrome)
Characteristic ECG finding suggesting - critical stenosis of the pLAD coronary artery
Develop Acute anterior wall MI within a few days to weeks (mean time of 8.5 days from the onset of
Wellens syndrome to infarction) in 75% of untreated patients
During an attack of chest pain the ST-segmentT-wave abnormalities usually normalize or develop into ST-
segment elevation
Initially respond well to medical management, but ultimately fare poorly with conservative therapy and
require revascularization strategies
Clinical and ECG criteria for
Wellenssyndrome
Biphasic or deeply inverted T waves in leads V2 and V3,
and occasionally in leads V1, V4, V5, and V6
No or minimal elevation of cardiac enzymes
No or minimal ST-segment elevation (< 1 mm)
No loss of precordial R-wave progression
No pathological precordial Q wave
A history of angina
Type A = Biphasic, with initial positivity
& terminal negativity (25% of cases)
Type B = Deeply and symmetrically
inverted (75% of cases)
Discussion
1st study: 26 /145 (18%) patients admitted for unstable angina had
this electrocardiographic pattern
- 12 /16 patients (75%) with ECG changes; who did not receive
coronary revascularization extensive anterior wall infarction
within a few weeks after admission
More specifically, 83% will have the lesion proximal to the second septal
perforator
performing ESTs for these patients can be fatal due to severe stenosis lead to
infarction at the time of increased cardiac demand
Clinical and risk factors data was collected by clinical evaluation and reviewing
hospital record from January 2011 to December 2011 for a total period of 12
months
Study populations consisted of patients with Wellens syndrome, age 30 years and
above, both genders who were undergoing coronary angiography for diagnostic or
revascularization purposes
Patients <30 years of age, those with a history of revascularization procedures (PCI
or CABG), with renal failure or with contraindications for coronary angiography
were excluded from study
Baseline demographics, clinical and risk factors data was collected from hospital record and by
interviewing patients
Only conventional risk factors including diabetes mellitus, hypertension,dyslipidemia, smoking and
family history for premature CAD as defined in operational definitions were assessed in this study
Elective coronary angiography was performed through standard femoral or radial artery approach
CAD was defined as >1 epicardial coronary segment with stenosis > 25% and was diagnosed visually
Patients were grouped as having single vessels disease (SVD), double vessel disease (DVD) and triple
vessel disease (TVD) according to the number of vessels involvement
30 (75%) males
LifeInTheFastLane.com
References
Wellens Syndrome
Ersan Tatli, Meryem Aktoz, Wellens syndrome: The electrocardiographic finding that is seen as
unimportant Cardiol J 2009; 16: 7375
De Zwann C, Bar FW, Janssen JH et al. Angiographic and clinical characteristics of patients with unstable
angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am
Heart J, 1989; 117: 657665.
Tandy TK, Bottomy DP, Lewis JG. Wellens syndrome. Ann Emerg Med. 1999 Mar. 33(3):347-51.
LMS/ LMCA Disease
Mohan Gamesh
The value of ST-segment elevation in lead
aVR for predicting left main coronary artery
lesion in patients suspected of ACS
Rom J Intern Med.2012 Apr-Jun;50(2):159-64.
Nough H,Jorat MV,Varasteravan HR,Ahmadieh MH,Tavakkolian N,Sheikhvatan M
Abstract
The use of lead aVR for predicting appearance of left main coronary artery (LMCA) lesion
evaluates the predictive value of ST-segment elevation in lead aVR on ECG in the
diagnosis of significant LMCA lesions
Methods
The study population consisted of 400 consecutive patients admitted within 6 hours from
the onset of typical chest pain to coronary care unit (CCU)
Electrocardiogram was recorded after the admission to emergency ward
ST segment elevation in aVR lead was measured and coronary angiography was
performed within 48 hours admission to CCU
RESULTS
31% of suspected patients had ST segment elevation in aVR lead that
elevation more than 0.1 mv was observed in 34.7% of all subjects
High incidence of ST segment elevation > 0.1 mv was seen in the
group with left main lesion so that 40.7% of men and 43.8% of
women with (LMCA) lesion had ST segment elevation > 0.1 mv. There
was a significant relationship between the incidence of ST segment
elevation > 0.1 mv and the number of diseased coronary vessels in
men. However, this relation was not observed in women. Different
risk profile of ACS did not influence the incidence of the ST-segment
elevation in aVR lead. Compared with coronary angiography, ST-
segment elevation in lead aVR in ECG had a sensitivity of 62.7%, a
specificity of 73.6%, a positive predictive value of 25.8%, and a
negative predictive value of 93.1% in predicting LMCA disease.
This ECG demonstrates the classical pattern of
left main coronary artery (LMCA) occlusion:
Widespread horizontal ST depression, most prominent in
leads I, II and V4-6
ST elevation in aVR 1mm
ST elevation in aVR V1
However, ST elevation in aVR is not entirely specific to
LMCA occlusion. It may also be seen with:
Proximal left anterior descending artery (LAD) occlusion
Severe triple-vessel disease (3VD)
Diffuse subendocardial ischaemia e.g. due to O2 supply/demand
mismatch,following resuscitation from cardiac arrest
NB.Some authorsargue that using the term LMCA occlusion is
inaccurate, as most of these patients have at least some flow in
their LMCA (i.e. incomplete LMCA occlusion); whereas a complete
LMCA occlusion would rapidly lead to STEMI, cardiogenic shock
and death.
Mechanism of STE in aVR
Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6;
therefore ST depression in these leads will produce reciprocal ST elevation in aVR.
Lead aVR also directly records electrical activity from theright upper portion of
the heart, including the right ventricular outflow tract and the basal portion of the
interventricular septum. Infarction in this area could theoretically produce ST
elevation in aVR.
ST elevation is aVR is therefore postulated to result fromtwo possible
mechanisms:
Diffuse subendocardial ischaemia,with ST depression in the lateral leads
producing reciprocal change n aVR (= most likely).
Infarction of the basal septum, i.e. a STEMI involving aVR.
The basal septum is supplied by the first septal perforator artery (a very proximal
branch of the LAD), so ischaemia / infarction of the basal septum would imply
involvement of the proximal LAD or LMCA.
Predictive Value of STE in aVR
In the context of widespread ST depression + symptoms of myocardial ischaemia:
STE in aVR 1mm indicates proximal LAD / LMCA occlusion or severe 3VD
STE in aVR 1mm predicts the need for CABG
STE in aVR V1 differentiates LMCA from proximal LAD occlusion
Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion
In the context of anterior STEMI:
STE in aVR 1mm is highly specific for LAD occlusion proximal to the first septal branch
In patients undergoing exercise stress testing:
STE of 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis
Magnitude of ST elevation in aVR is correlated with mortality in patients with acute
coronary syndromes:
STE in aVR 0.5mm was associated with a 4-fold increase in mortality
STE in aVR 1mm was associated with a 6- to 7-fold increase in mortality
STE in aVR 1.5mm has been associated with mortalities ranging from 20-75%