Case Report: Point of care ultrasound of a broken heart

By Winnie Chan, MD, FRCPC and Joseph Newbigging, CCFP(EM), FCFP

Queen’s University, Kingston Ontario

 


Download article PDF – POCUS Journal 2017; 2(1):02-03


 

Clinical case

Mrs. K, a 70 year old lady, presented to the urgent care with severe retrosternal chest pain that started at rest. She described the pain as a constant heaviness and rated it as 9/10 in severity. The pain did not radiate to the neck, arms, or back. The pain had started one hour after she was informed that her son had passed away unexpectedly. She denied any associated shortness of breath, nausea, diaphoresis, or presyncope. There was no relief with nitroglycerine spray. Mrs. K denied any previous episodes of similar chest discomfort. Her only cardiac risk factor was dyslipidemia. Her other comorbidities included gastroesophageal reflux disease and a previous hip arthroplasty.

Mrs. K was hemodynamically stable on presentation. Her blood pressure was 147/93, heart rate 96 BPM, RR 22 breaths per minute, oxygen saturation (SPO2) 100% on room air, afebrile. She had a normal physical exam and was euvolemic. Her initial ECG showed 0.5 mm of ST elevation in aVL (online Figure S1). There was no evidence of ST depression or T wave inversions. Q waves were present in the right precordial leads (V1 to V3). There were no pathologic ST or T wave changes in these leads. These Q waves were new since her last documented ECG in 2007. Her QT interval was 462ms. The 15 lead ECG did not show any additional pathology. Serial ECGs over the next two hours did not show any dynamic changes, however, there was further prolongation of the QT to 503 ms. Her initial chest x-ray was normal. Her initial high sensitivity troponin was 2355 ng/L (Normal <30ng/L) and CK was 512 U/L (Normal 35-164U/L).

 

Figure S1. Initial ECG showing a normal sinus rhythm. Normal axis. Mildly prolonged QTc at 462 ms. Q waves are present in the right precordial leads (V1-V3). 0.5 mm of ST elevation in aVL.

 

Clinical dilemma

Mrs. K presented with visceral chest pain and troponin raise. The most likely diagnosis accounting for her presentation was acute coronary syndrome. Myocarditis, acute pulmonary embolism, and aortic dissection were other possibilities in the differential, although atypical for this type of presentation. The temporal relationship between the onset of chest pain and acute emotional stressor raised the suspicion of a possible Takotsubo syndrome. Looking at prevalence alone, the diagnosis of acute coronary syndrome was more likely. Takotsubo syndrome accounts for approximately 1-2% of all patients who present with suspected acute coronary syndrome or ST- elevation myocardial infarction [1]. Both Takotsubo syndrome and acute coronary syndrome would be expected to present with wall motion abnormalities.

Indication for point of care ultrasound

  1.  Assess for left ventricular wall motion abnormalities (Table 1)
  2.  Screen for other cardiac emergencies which would present with chest pain

 

Table 1. Image acquisition (Note: All images were acquired using general radiology convention, used frequently in emergency medicine.  Screen index marker is on the left)

 

Image interpretation

The apical four-chamber view (Figure 1, online video S1) showed moderate reduction of left ventricular systolic function. There was akinesis/hypokinesis of the mid inferoseptal and anterolateral segments and the apex. The base appeared hyperdynamic. Right ventricular size and systolic function were normal.

The parasternal long axis view (online video S2) similarly showed a hyperdynamic base with mid anteroseptal akinesis. The inferolateral basal and mid segments were contracting normally.

The parasternal short axis view (online video S3), taken at the papillary muscle level, demonstrated diffuse hypokinesis/akinesis. Only the inferolateral segment in this view was contracting normally.

The subcostal view (online video S4) did not demonstrate any pericardial effusion and the right ventricle systolic function appeared normal.

 

Figure 1. Four chamber view. These images were taken in diastole (A) and systole (B) which demonstrates regional wall motion abnormalities. The mid and apical segments are akinetic. The base is the only area contracting in this view. This leads to the appearance of apical ballooning.

 

 

Clinical synthesis

Through the integration of all the cardiac views obtained, the following was concluded:

  1. There was moderate left ventricular systolic dysfunction.
  2. There were regional left ventricular wall motion abnormalities (WMAs)s involving almost all mid and apical segments.
  3. The base of the left ventricle was hyperdynamic.
  4. There was no pericardial effusion to suggest pericarditis.
  5. The right ventricle was normal in size and function arguing against a submassive or larger pulmonary embolus.

It was thought that the regional left WMAs involved could have been the result of an acute coronary syndrome. However, a single culprit artery would be unlikely to cause all of these acute WMAs, as the regions involved are typically perfused from multiple arteries. Even though ACS was the most important diagnosis to pursue, the pattern of WMAs was quite characteristic of the apical variant of Takotsubo cardiomyopathy. There are other variants of Takotsubo including mid, basal, focal, and global type; however, the apical type is the most common and the estimated prevalence is 50-80% [1].

Vignette resolution

In this instance, point of care ultrasound demonstrated regional wall motion abnormalities which made us suspect acute coronary syndrome or Takotsubo syndrome over other causes of acute retrosternal chest pain. The troponin and CK values peaked at 3209 ug/L (Normal <30ng/L) and 512 U/L (Normal 35-164U/L) respectively. Although Takotsubo syndrome was suspected, acute coronary syndrome must first be ruled out. Therefore, the case was discussed with the interventional cardiologist and a coronary angiogram was performed. It demonstrated normal coronary anatomy with minor luminal irregularities. Mrs. K was diagnosed with Takotsubo syndrome following the angiogram.

Conclusions

Mrs. K’s presentation was quite classic for Takotsubo syndrome, also known as broken heart syndrome or stress-induced cardiomyopathy. This condition was named Takotsubo because the left ventricular apical ballooning at end-systole resembles a Japanese octopus trap. Patients with Takotsubo syndrome present with chest pain frequently associated temporally with an emotional or physical stressor. They do not have culprit lesions on angiography to explain the observed wall motion abnormalities. The 2015 Heart Failure Association of the European Society of Cardiology (HFA) Takotsubo Syndrome Diagnostic Criteria are shown in Table 2 [1].

 

Table 2. Heart Failure Association diagnostic criteria for Takotsubo syndrome (Reproduced with permission from Lyon et al. 2016 [1])

 

The diagnosis of Takotsubo syndrome is felt to be a diagnosis of exclusion and requires that acute coronary syndrome be ruled out. Often, Takotsubo presents with ST-changes that are indistinguishable from an acute ST elevation myocardial infarction or a high-risk NSTEMI. These patients should be referred for urgent evaluation by a Cardiologist. Patients who meet criteria for reperfusion strategies should be referred for urgent coronary angiography or consideration of fibrinolytic therapy in places without urgent angiography.

Point of care focused cardiac ultrasound can be a useful tool in the assessment of patients with chest pain. Focused cardiac ultrasound can be used to look for findings which are often seen in many emergency causes of chest pain including left ventricular dysfunction, right ventricular dysfunction, and pericardial effusion. The presence or absence of these findings can be used by physicians to guide their clinical decision making.

 

References

  1. Lyon AR, Bossone E, Schneider B, Sechtem U, et al. Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. European journal of heart failure, 2016; 18(1):8-27.

Leave a Reply

Your email address will not be published. Required fields are marked *