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CASE REPORT
Year : 2022 | Volume
: 32
| Issue : 3 | Page : 175-176
Global longitudinal strain in wellens' syndrome
Rakesh Agarwal1, Aditya Verma2
1 Department of Cardiology, Vedant Hospital, Thane, Maharashtra, India
2 Department of Cardiology, Institute of Postgraduate Medical Education and Research and SSKM Hospital, Kolkata, West Bengal, India
Correspondence Address:
Rakesh Agarwal
Lodha Splendora, Tierra B, 2502, Thane, Maharashtra
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jcecho.jcecho_13_22
We present the case of a young man with “noncardiac” chest pain, subsequently diagnosed as Wellens' syndrome. We report the early changes in left ventricular global longitudinal strain imaging findings in these patients despite preserved ejection fraction, and review the features associated with this stereotypical cardiac condition. The patient underwent a successful percutaneous coronary intervention.
Keywords: Wellens, global longitudinal strain in Wellens, echocardiography in Wellens
Wellens' syndrome refers to a preinfarction state characterized by characteristic electrocardiography (ECG) changes, and has a chance of progression to acute anterior wall myocardial infarction. Echocardiography in a case of Wellens' syndrome is normal and reveals normal left ventricular (LV) systolic function. We report the case of a patient with stereotypical Wellens' syndrome and decreased LV global longitudinal strain (GLS). We show that despite having gross normal ejection fraction, LV systolic function becomes deranged initially as reflected in GLS values. We also review the literature associated with this condition.
Case ReportA physically active 42-year-old man presented with chest discomfort for 2 days. He had previously been seen by a physician and was diagnosed as “noncardiac chest pain.” The patient described the pain as being localized to the left parasternal area, and described it as a heaviness that “comes and goes.” He was a known hypothyroid and was on oral levothyroxine supplementation (75 μg/day). He had been a smoker for 20 years now and had smoked over 30 pack-years. He had a strong family history of cardiac disease in that his four uncles on the paternal side had died to heart attack. On admission, he was clinically stable with normal hemodynamic parameters.
On the basis of the clinical presentation of chest discomfort in a young smoker, differential diagnosis of acute coronary syndrome (ACS), acute pulmonary embolism, and noncardiac causes of chest pain was made.
Clinical examination revealed no specific findings. His heart rate was 60 beats/min and blood pressure was 130/78 mmHg. A resting 12-lead ECG was obtained [Figure 1] which revealed sinus rhythm, sinus bradycardia, and biphasic T-wave inversion in leads I, aVL, and V2-V5. Cardiac troponins were obtained which were negative. The patient underwent an echocardiography which revealed no regional wall motion abnormality and a preserved LV systolic function (LV ejection fraction ~ 65%). A LV strain imaging was obtained which revealed severely decreased LV strain values in the basal and mid-basal anterior septum and anterior wall segments [Figure 2]. The GLS value was −11.3%.
In view of his clinical and noninvasive findings, the patient was taken up for cardiac catheterization and an invasive coronary angiography was performed. It revealed critical stenosis in the mid-left anterior descending (LAD) artery with likely superimposed thrombosis. A drug-eluting stent 3.5 mm × 28 mm stent was inflated in the culprit vessel. The patient reported a reproduction of his chest pain during stent balloon inflation with resolution once the stent balloon was deflated. Some under expansion of the stent were noted on the postpercutaneous transluminal coronary angioplasty segment which was dilated with a 4 mm × 8.0 mm NC balloon. Subsequently, the patient was shifted to the intensive care unit for 24 h for observation.
The patient had an uneventful stay and was discharged after 48 h with advice on risk factor modification. His discharge medications included dual antiplatelet therapy with aspirin and ticagrelor, a statin, and an angiotensin-converting enzyme inhibitor.
DiscussionChest pain, even in the young, should always be evaluated with an astute clinical eye to avoid missing serious disease. Our patient was a healthy 42-year-old man with an atypical chest pain with classical features of Wellens' Type A syndrome.
Wellens' syndrome refers to a preinfarction state of the LAD coronary artery and constitutes as many as 14%–18% of all unstable angina presentations.[1] It is characterized by a transient occlusion of the LAD due to plaque rupture. This leads to occlusion of the LAD, leading to ACS-like presentation. However, subsequent spontaneous clot lysis or disruption of the occlusion prevents a full-blown ST-elevation myocardial infarction from occurring.[2]
Diagnosis of Wellens' syndrome is made on the basis of ECG findings, clinical presentation, and biochemical investigations. Diagnosis entails demonstrating:
Biphasic or monophasic deep T-wave inversions in leads V2-V3 (however, leads V1-V6 may be involved) ANDAbsent or minimal (<1 mm) ST elevationAbsent Q-waves and normal R-wave progressionECG pattern persists when the patient is free from anginaHistory of recent anginal chest pain with normal or only mildly raised cardiac biomarkers.The biphasic (initially positive T-wave followed by negativity) T-wave inversion pattern is referred to as Wellens' Type A while deep T-wave inversion is called Type B pattern.[1],[2]
Diagnosis of Wellens' syndrome requires immediate catheterization and percutaneous coronary intervention owing to the unstable nature of the condition. Managed at the right time, it can prevent progression to an acute anterior wall myocardial infarction and thus save considerable morbidity and mortality.
Through our case, we have demonstrated that despite having a normal echocardiography, patients with Wellens' syndrome have decreased LV GLS values reflecting subclinical dysfunction. It is now well known that GLS values can predict long-term cardiovascular mortality and morbidity.[3]
ConclusionWellens' syndrome is a life-threatening emergency and must be tackled as a routine ACS case. Despite having normal LV function, these patients develop subclinical LV dysfunction as demonstrated by reduced longitudinal strain values. A quick intervention may prevent these patients from landing into permanent damage to the LV.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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