A 42-year-old Female with Worsening Chest Tightness & Dyspnoea
A 42-year-old female presented to the hospital with a 2-day history of fever (39.3°C), worsening dyspnoea, chest tightness, reduced exercise capacity and dizziness. On further questioning it is revealed that her dyspnoea and chest tightness started 10 months ago and have been getting progressively worse. She says she experienced similar symptoms of chest pain 4 years ago but wasn’t investigated further as her symptoms subsided.
On this admission, bloods showed Hb 87, Troponin 10.05, NT pro-BNP 1,118, CRP <5.0. U&Es, LFTs & Bone Profile were all normal. An ECG was performed which showed poor R-wave progression in the anterior wall. Transthoracic echocardiogram (TTE) was also performed which showed regional wall motion abnormality of the left ventricle with reduced LVEF (32%) and an enlarged left ventricular end-diastolic diameter (67mm). Cardiac MRI was then performed to further evaluate the heart. Following these investigations, the patient underwent coronary angiography and eventually coronary artery bypass graft (CABG).
From left to right: 1) TTE results 2) Coronary angiography finding of woven coronary artery 3) Cardiac MRI showing infarction of the apex 4) Blood test results
-
This patient was admitted with an acute decompensation of an underlying chronic heart failure. The patient has progressive shortness of breath with a raised NT Pro-BNP which should raise suspicions for heart failure. The TTE finding of reduced LVEF should further confirm your suspicion of this diagnosis. They likely suffered a myocardial infarction (MI) some years ago as is evidenced by the ECG findings of poor R-wave progression and the TTE/cardiac MRI finding of regional wall motion abnormality, with the heart failure developing slowly over time as a complication of this MI. The finding of a low Troponin level also supports this and indicates that the MI isn’t an acute finding.
The finding of poor R-wave progression on ECG is suggestive of a prior anterolateral infarction, further cementing this diagnosis. However, it is worth mentioning that this finding can also be seen in LVH, RVH, cardiomyopathy and can also be a normal variant.
Assessment of regional wall motion is an important aspect of every echocardiogram. Regional wall motion abnormalities (RWMAs) are defined as regional abnormalities in contractile function of the myocardium, with ischaemia/infarction being the most common cause. All types of ischaemia (acute, subacute, chronic) result in temporary RWMAs, however, if the ischaemia carries on for an extended period of time (i.e. >20mins) then the tissues become infarcted resulting in permanent RWMAs.
References:
1) https://litfl.com/poor-r-wave-progression-prwp-ecg-library/
3) https://lms.resus.org.uk/modules/m15-v2-acute-coronary/11118/resources/chapter_4.pdf
-
The diagnosis of chronic heart failure should be suspected based off your history and physical examination of the patient and confirmed with an NT Pro-BNP and echocardiogram showing either reduced ejection fraction (HFrEF), or if the ejection fraction is preserved but there is abnormal end-diastolic filling then this would indicate heart failure with preserved ejection fraction (HFpEF).
NICE guidelines advise referral for specialist assessment & echocradiography based off the NT Pro-BNP findings:
NT Pro-BNP <400 —> HF unlikely, consider alternative diagnosis
NT Pro-BNP 400-2000 —> refer patient to be urgently seen within 6 weeks
NT Pro-BNP >2000 —> refer patient to be urgently seen within 2 weeks
In addition, NICE recommends additional investigations such as ECG, chest X-Ray, urinalysis, PFTs & a complete set of bloods to fully investigate the patient.
References:
1) https://www.nice.org.uk/guidance/ng106/chapter/Recommendations
-
Acute Heart Failure refers to an episode of acute decompensation of an already existing Chronic Heart Failure. This episode is characterised by signs and symptoms of volume overload, including peripheral pitting oedema, pulmonary oedema (manifesting as severe shortness of breath with fine crackles on auscultation), raised JVP, fatigue and possibly syncope. Treatment of this acute episode primarily involves diuresing the patient using IV diuretics (e.g. Furosemide) followed by a step-down to roal diuretics once the patients symptoms are better under control. U&Es should be carefully monitored during this time to ensure that profound electrolyte disturbances don’t develop.
Once the acute episode is resolved, the patient needs to continue with medication to manage their chronic heart failure.
References:
1) https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations#initial-pharmacological-treatment
-
According to the NICE guidelines, first-line treatment of chronic heart failure involves prescribing both an ACE-inhibitor (ACE-I) as well as beta-blocker (BB).
If an ACE-I is contraindicated then an ARB can be prescribed instead. A mineralocorticoid receptor antagonists (MRA) can be offered in addition to to an ACE-I & BB to people who have HFrEF if their symptoms continue.
If symptoms still persist despite first-line treatment (ACE-I/ARB + BB + MRA), seek specialist advice and consider one or more of the following:
replace ACE-I/ARB with sacubitril valsartan if EF <35%
Add ivabradine for sinus rhythm with HR >75bpm and EF <35%
Add hydralazine and nitrate (especially if of Afro-caribbean descent)
Add digoxin for HF with sinus rhythm to improve symptoms
Measure U&Es to assess renal function before and after starting a new medication and after each dose increment. Special consideration should be taken in patients with confirmed renal failure/kidney dysfunction.
Implantable cardioverter defibrillators and cardiac resynchronisation therapy can be considered in patients who develop arrythmia.
References:
2) https://www.nice.org.uk/guidance/ng106/chapter/Recommendations
-
All people with chronic heart failure need monitoring. This monitoring should include:
a clinical assessment of functional capacity, fluid status, cardiac rhythm (minimum of examining the pulse), cognitive status and nutritional status,
a review of medication, including need for changes and possible side effects and
an assessment of renal function.
This is a minimum. More detailed monitoring will be needed if the person has significant comorbidities or if their condition has deteriorated since the previous review. The monitoring interval should be short (days to 2 weeks) if the clinical condition or medication has changed. However, if the patient’s condition is stable then twice annual follow-up is normally sufficient.
References:
-
Whilst this patient didn’t have an acute infarction, it is important to do a full diagnostic workup of their heart to understand what the cause of their heart failure is. In this case, in addition to ECG and TTE, a cardiac MRI was also performed which showed definitive proof of a transmural infarction at the heart apex. Following this finding, the patient needed to undergo coronary angiography to assess for any underlying coronary artery disease (CAD). Once CAD was confirmed in this patient their risk level was then assessed and they were evaluated as being high risk for suffering future adverse cardiac events (i.e. repeat MI). Hence CABG was offered and performed.
References:
1) https://www.nice.org.uk/guidance/ipg377/chapter/2-The-procedure
-
The original article mentions that “woven coronary arteries,” (WCA) were found when performing this patient’s coronary angiogram. WCA is a rare congenital anomaly in which a coronary artery is divided into thin channels that merge again into the distal lumen. The pathogenesis of WCA has not been elucidated, but most scholars believe that a congenital malformation is the most likely cause. Whilst this condition was intially thought to be benign, we have incerasingly learned over the years that WCA is not a completely benign disease: it may be asymptomatic, or it may be accompanied by chest pain, myocardial ischemia, myocardial infarction and even sudden cardiac death.
So whilst this patient’s HF has likely developed as a long-term complication of her previous MI. It is also possible that the initial MI occured secondary to this congenital abnormality of her coronary arteries (or at least they may have contributed to disease progression).
References:
1) https://www.ahajournals.org/doi/10.1161/CIRCINTERVENTIONS.119.008087
2) https://academic.oup.com/eurheartjsupp/article/24/Supplement_K/suac121.286/6911435
Source: https://doi.org/10.3389/fcvm.2022.1034860
Case Summary & Questions written by Dr Ahmed Kazie
If you have any feedback for us on this clinical case then please feel free to send us an email at: teaching.happymedics@outlook.com
Disclaimer:
The following case study summary and questions have been published by Happy Medics for educational purposes. The content and the case study material included in this publication are not owned by the author of this website. The original article can be found at the following link: https://doi.org/10.3389/fcvm.2022.1034860
While every effort has been made to ensure the accuracy of the content listed on the website, the author and company make no guarantees of the accuracy and reliability of the content within. The content is intended solely for educational purposes and is not meant to diagnose or treat actual patients. Individual patients should be treated on a case-by-case basis using the most up-to-date guidelines and under the supervision of an appropriately trained physician.
It is important to note that all Frontiers articles from July 2012 onwards are published with open access under the Creative Commons CC-BY license (the current version is CC-BY, version 4.0). This means that the author(s) retains copyright, but the content is free to download, distribute, and adapt for commercial or non-commercial purposes, given appropriate attribution to the original article.
Please ensure proper attribution is given to the original article and comply with the terms of the Creative Commons CC-BY license when using the content for any purpose.
https://www.frontiersin.org/guidelines/policies-and-publication-ethics
