Acute myocardial injury with normal coronary arteries in a young male: a case report of aortic dissection with rapidly progressive aortic regurgitation

Abstract

Type A aortic dissection (TAAD) is a life-threatening condition that often presents diagnostic challenges, particularly when mimicking acute myocardial infarction (AMI). This case report describes a 31-year-old male with a history of fever and no cardiovascular history who presented with acute chest pain and rapidly developed hemodynamic instability. Initial assessments revealed mild aortic regurgitation (AR) and ascending aortic dilation but no aortic dissection was reported. ECG showed ST-segment changes, yet coronary angiography ruled out obstructive coronary disease. Serial daily echocardiograms demonstrated rapid progression of AR from mild to severe within 72 h, accompanied by worsening left ventricular dysfunction. Reassessment of aortic CT confirmed TAAD with left main coronary artery involvement. Different elements of his presentation suggested possible other diagnoses, including TAAD, AMI and myocarditis. We discuss how evaluating these other diagnostic possibilities led to the correct diagnosis. This case underscores the diagnostic pitfalls of TAAD masquerading as AMI, it demonstrates the need to consider aortic dissection in patients with AMI and/or emerging diastolic murmurs of AR.

Introduction

Acute Aortic Syndrome (AAS) are lethal conditions requiring rapid diagnosis and intervention, and aortic dissection is the most common of the AAS [1]. The annual incidence of aortic dissection ranges from 5 to 30 cases per million population, with men more commonly affected, while the majority of aortic dissections occur in individuals aged 50 to 70 years [1–3]. Aortic dissection can lead to a number of complications, including extensive myocardial ischemia, acute aortic regurgitation (AR), cardiac tamponade, stroke, or malperfusion syndromes [2]. These complications concomitant with type A aortic dissection (TAAD) may obscure the diagnosis, especially in younger patients without a prior history of cardiovascular disease. TAAD with left main coronary artery (LMCA) involvement is a rare but lethal condition associated with low output syndrome, which results from extensive myocardial necrosis, even after technically successful aortic repair [4, 5]. Accurate diagnosis of TAAD prior to ruling out acute myocardial infarction (AMI) remains challenging, particularly in hemodynamically unstable patients [5]. Early identification of clinical signs and symptoms to achieve prompt diagnosis is pivotal for improving prognosis in such critical cases.

We present a complex case of localized ascending aortic dissection complicated by severe aortic regurgitation, cardiac dysfunction due to LMCA ischemia, and a left atrial thrombus. Following confirmation of the diagnosis, the patient underwent surgical repair of the aorta, aortic valve repair, and coronary ostial reconstruction. Postoperatively, a percutaneous ventricular assist device (TeleHeart P50) was implanted for left ventricular support.

Case report

Whispers of disease: initial presentation with acute chest pain

A 31-year-old man with no known medical history presented to the emergency department of a local secondary hospital with almost 1 h of acute-onset chest pain. He also reported a 3-day history of fever, but the highest body temperature was unknown. Initial transthoracic echocardiography (TTE) demonstrated mild aortic regurgitation, dilation of ascending aortic (41 mm), and preserved left ventricular ejection fraction (LVEF). Aortic computed tomography angiography (CTA) revealed bilateral pulmonary infiltrates and a small pericardial effusion, but no evidence of aortic dissection was reported. However, his condition rapidly deteriorated two hours later, manifested as worsening chest pain, altered mental status and hypoxemia (SpO2 80%). Electrocardiography (ECG) showed extensive ST depression in inferior /anterior /lateral leads and ST elevation in lead aVR. Troponin I was slightly elevated (0.09 ng/mL). Arterial blood gas analysis revealed severe hypoxemia (PaO2 37.6 mmHg). The patient was urgently intubated and transferred to a better hospital.

Unmasking the cascade: From STEMI-mimicking ST elevation to acute severe aortic regurgitation

Upon arrival at the emergency department, a series of examinations and laboratory findings were consistent with the manifestations of acute coronary syndrome (ACS). These included ST-segment elevation with upward convexity in leads aVR and V1, significant ST-segment depression in the inferior, anterior, and anterolateral leads, left anterior fascicular block, and impaired left ventricular wall motion (LVEF 40%) (Fig. 1A; Table 1). Emergency coronary angiography was subsequently performed; however, it revealed no evidence of obstructive coronary artery disease (Fig. 2). Notably, ECG showed significant improvement following the procedure (Fig. 1B).

Fig. 1.

(A) Upon admission to the tertiary care hospital’s emergency department, an ECG was recorded. It revealed greater ST-segment elevation in lead aVR than in V1, a pattern strongly suggestive of a left main coronary artery lesion, which prompted the decision to perform emergency PCI. (Red arrows: ST-segment elevation; Blue arrows: ST-segment depression.) (B) The 2-hour post-PCI ECG showed marked improvement versus pre-PCI, with ST-segment normalization, residual T-wave abnormalities, and poor R-wave progression. ECG, electrocardiographic; PCI, percutaneous coronary intervention

Table 1.

Trends in Key Imaging and Laboratory Parameters

	Reference ranges	Day1	Day2	Day3
Echocardiographic
Aortic Regurgitation	none	mild to moderate	moderate to severe	moderate to severe
Pericardial Effusion (mm)	None; <3	None	Ant: 5.7; Inf: 7.2	Ant: 5.0; Post: 6.3
LVEF (%)	52.6-76.2 [6]	40	36	38.9
Laboratory Parameters
Troponin-T (ng/mL)	< 0.014	0.187	1.19	2.84
CK-MB (U/L)	< 24	51	395	319
BNP (pg/mL)	< 100	105	1325	1568
WBC (×10⁹/L)	4–10	14.5	17.1	14.8
CRP (mg/L)	< 10	20.3	20.7	49.7
IL-6 (pg/mL)	< 7	NA	51.67	145.6
D-dimer (mg/L)	< 0.5	1.14	0.81	1.6

LVEF, left ventricular ejection fraction; CK-MB, creatine kinase-MB; BNP, B-type natriuretic peptide; WBC, white blood cell count; CRP, C-reactive protein; IL-6, interleukin-6; Ant, Anterior; Inf, Inferior; Post, Posterior; NA, not available

Fig. 2.

The coronary angiography result is negative. (A) Right coronary artery. (B) Left coronary artery

Serial daily TTE demonstrated rapid progression of aortic regurgitation from mild to severe over a 72-hour period. Viral serology (including Coxsackievirus IgM, CMV DNA, EBV DNA) and autoimmune panels (such as antinuclear antibodies) were unremarkable. Despite aggressive management, clinical deterioration necessitated transfer to a tertiary care center for advanced evaluation.

The decisive clue: CTA identifies acute aortic dissection

Three days later, the patient was transferred to a high-volume regional tertiary care hospital. Subsequent bedside TTE revealed a suspicious dissection flap in the ascending aorta, separating the true from the false lumen, with the dissection extending to the aortic valve (notably the left coronary ostium). The findings included eccentric severe aortic regurgitation, segmental left ventricular wall motion abnormalities (suggestive of left coronary artery involvement), and moderate mitral regurgitation. An urgent CTA confirmed a TAAD without involvement of the aortic arch branches, but with a left atrial thrombus (Fig. 3). Laboratory results showed troponin-T 3.55 ng/mL and D-dimer 1.28 mg/L.

Fig. 3.

Aortic computed tomography angiography confirmed a Stanford type A aortic dissection and a left atrial thrombus. (A) The ascending aorta is normal. (B) Local dissection of aorta involving the left coronary ostium (red arrow); a left atrial thrombus (blue arrow). (C) 3-dimensional imaging

Emergency surgery was performed, including ascending aortic replacement, aortic valve repair, left atrial thrombectomy, and left atrial appendage closure. Intraoperative findings confirmed left coronary ostial involvement, necessitating coronary ostial reconstruction. Postoperatively, a percutaneous ventricular assist device (TeleHeart P50, the first domestic case report of its application in emergency aortic dissection surgery) was implanted for left ventricular support due to diffuse reduced left ventricular activity (LVEF 26%), and coronary angiography confirmed patent coronary ostia. The patient experienced an uninterrupted recovery postoperatively, culminating in discharge and a return to baseline activities of daily living with complete autonomy.

Follow-up

Postoperative CTA showed no evidence of residual dissection and confirmed patent coronary ostia. Serial TTE performed at 0.5, 1, 2, 4, and 7 months postoperatively consistently demonstrated trace aortic regurgitation. Although short-term TTE evaluations up to 4 months revealed persistently reduced LVEF (18.1% − 28.1%) and impaired left ventricular function, with apical aneurysm formation first detected at the 2-month follow-up, the 7-month TTE showed marked improvement in LVEF, which increased to 45.2%. The apical aneurysm remained stable in size without further expansion or thrombus formation. The patient has now regained complete capacity for activities of daily living.

Discussion

We believe the lessons of this case are multiple, including that (a) type A aortic dissection (TAAD) may manifest with acute myocardial infarction (AMI)-like presentations or heart failure secondary to aortic regurgitation (AR). In patients with negative coronary angiography findings, immediate screening for aortic dissection is imperative. (b) TAAD mimicking acute myocardial infarction poses significant diagnostic challenges, frequently leading to increased mortality rates due to delayed diagnosis. Establishing an optimal therapeutic strategy remains clinically challenging under such circumstances. (c) Myocarditis should never be diagnosed unless the patient meets the existing clinical criteria, as this may lead to overlooking alternative etiologies. (d) New-onset diastolic murmur of AR is never normal and necessitates urgent investigation for underlying aortic dissection. (e) For patients presenting with TAAD, who are stable enough for transfer or with multiple comorbidities for whom intervention is considered, referral to a high-volume center is reasonable to optimize treatment outcomes.

TAAD can lead to a range of complications, including extensive myocardial ischemia, AR, and cardiac tamponade. Coronary malperfusion can be attributable to compression of the coronary arteries by a hematoma or the dissection flap [2]. The Neri classification categorized three main types of coronary artery lesions secondary to aortic dissection (AD) [4]. The reported incidence of coronary malperfusion in acute AD ranges from 6.1% to 14.1% [7]. Moreover, patients with coronary involvement demonstrate increased prevalence of aortic regurgitation (AR). While right coronary artery (RCA) involvement is more frequent in AD, left main coronary artery (LMCA) compromise shows significant association with cardiac arrest [8, 9]. The ubiquity of CT angiography (CTA), combined with rapid acquisition of intuitive 3-dimensional (3D) imaging data sets, has led to its wide adoption for the assessment of suspected aortic anatomy and pathology [10]. However, in critically ill patients presenting with ST-segment elevation myocardial infarction (STEMI) and cardiogenic shock, CTA imaging is often deferred in favor of immediate coronary reperfusion therapy. Beside TTE can be useful in the evaluation of patients with TAAD to detect complications, including aortic valve regurgitation, left ventricular dysfunction, and cardiac tamponade [11]. However, it is a limited screening technique in some low-volume center because of the unavoidable operator dependency, reduced image resolution, and limited field of view. Some studies emphasize the use of intravascular ultrasound (IVUS) during AMI intervention because its characteristic findings of coronary compression may enable immediate identification of TAAD [8].

While early revascularization is recommended for AMI complicated by cardiogenic shock, it may delay diagnosis and aortic repair surgery in patients with underlying TAAD [12]. Coronary involvement in TAAD is universally associated with increased mortality, potentially attributable to delayed diagnosis and antiplatelet therapy. Currently, case reports occasionally describe successful bridging to TAAD surgical repair in patients with acute aortic dissection and persistent myocardial ischemia accompanied by hemodynamic instability through stent implantation [13–15]. Although these interventions may stabilize critically ill patients temporarily, they do not address the aortic dissection and serve only as temporary solutions. Some studies have also evaluated the benefits of preoperative coronary angiography for diagnosing coronary artery involvement [14]. However, this approach has not influenced the rate of coronary artery bypass grafting (CABG) nor improved outcomes in these patients. Interestingly, it has even been observed that such investigations may cause critical delays in treatment, as postponing surgical repair could lead to aortic dissection progression or rupture. The mortality rate of unoperated TAAD is 1%/h¹. Moreover, perioperative stent thrombosis is a severe complication linked to significantly increased mortality, particularly in cases of left main coronary artery (LMCA) stenting [16]. This complication arises from interrupted antiplatelet therapy and the prothrombotic state induced by surgery. Notably, patients on dual antiplatelet therapy (DAPT) exhibit significantly increased intraoperative and postoperative bleeding [17]. However, premature discontinuation of DAPT may lead to stent thrombosis. Currently, suspected or diagnosed acute TAAD requires urgent surgical evaluation. Surgical intervention can mitigate the immediate risk of aortic rupture/tamponade and correct myocardial ischemia and AR [18]. The efficacy of preoperative PCI for patients with TAAD accompanied by persistent myocardial ischemia and hemodynamic instability has not been determined. But recent series showed potential to improve outcomes by establishing end-organ perfusion (including cardiac) using endovascular means, before open central aortic repair (the time for subsequent open repairs will be determined based on a case-by-case basis) [19].

In retrospect, the initial CTA and TTE showed no evidence of aortic dissection. Due to hemodynamic instability necessitating endotracheal intubation, characteristic symptoms such as chest pain or tearing back pain was unobtainable. Both ECG and myocardial enzyme spectrum indicate AMI, so the key plan was to admit him to the AMI service for coronary reperfusion. However, the coronary angiogram was negative. Although a 3-day history of fever was a possibility for myocarditis, CTA was unfortunately not repeated to assess the presence of aortic disease, especially he had diastolic murmurs of aortic insufficiency. The patient developed worsening chest pain followed by hemodynamic instability. Notably, ECG showed significant improvement after coronary angiography. This clinical course raises the possibility of transient LMCA compromise secondary to TAAD, where the angiographic catheter may have inadvertently restored true lumen patency, leading to temporary coronary reperfusion. In a case series reported by Taguchi et al. involving nine patients with LMCA malperfusion in TAAD [14], four cases of severe cardiogenic shock ultimately resulted in death despite receiving venoarterial extracorporeal membrane oxygenation (VA-ECMO) as bridging therapy. Among these, three patients underwent stent implantation, while one procedure failed due to the inability to advance the guidewire into the true lumen. The remaining five patients were immediately transferred to the operating room for central repair following stent implantation, and all survived—including two who had been diagnosed with TAAD prior to angiography. Overall, only 22% of the patients received a TAAD diagnosis before coronary angiography was performed.Emergency physicians must recognize unusual clinical manifestations of aortic dissection (aortic diastolic murmur, mimicking acute myocardiac infarction, widening of the ascending aorta) and the role of shared decision making by multidisciplinary teams. In critically ill patients, any patient with these findings deserves urgent investigation for underlying aortic dissection. And for patients presenting with acute TAAD, who are stable enough for transfer or with multiple comorbidities for whom intervention is considered, referral to a high-volume center is reasonable to optimize treatment outcomes [20].

Abbreviations

TAAD

Type A aortic dissection

AMI

Acute myocardial infarction

AR

Aortic regurgitation

AAS

Acute aortic syndrome

LMCA

Left main coronary artery

TTE

Transthoracic echocardiography

LVEF

Left ventricular ejection fraction

CTA

Computed tomography angiography

ECG

Electrocardiography

ACS

Acute coronary syndrome

AD

Aortic dissection

RCA

Right coronary artery

STEMI

ST-segment elevation myocardial infarction

IVUS

Intravascular ultrasound

CABG

Coronary artery bypass grafting

DAPT

Dual antiplatelet therapy

VA-ECMO

Venoarterial extracorporeal membrane oxygenation

Author contributions

Dongdong Wei and Zhanglong Hu wrote the main manuscript text. Tao Zhang prepared Figs. 1, 2 and 3. Minjian Kong approved the final version to be published. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no Funding.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

This study was reviewed and approved by the Institutional Review Board / Ethical Committee of the Second Affiliated Hospital of Zhejiang University School of Medicine. Written informed consent was obtained from the patient for participation in this study.

Consent for publication

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.