An Unexpected Cause of Marathon Dyspnea: A Diagnostic Challenge in an Amateur Athlete

Introduction

Exertional symptoms that occur in amateur athletes during and after intense exercise can be nonspecific. Moreover, they can be difficult to interpret, given the above-average exercise capacity and high thresholds for symptoms in this population, which can in turn provide false reassurance regarding the absence of significant coronary artery disease (CAD).

If individuals with very high exercise capacity (achieving ≥10 metabolic equivalents [METs]) report any symptoms, these can occur during extreme exertion, which is difficult to correlate with the conventional Canadian Cardiovascular Society anginal scale scores for ordinary activities such as walking or climbing stairs in patients with average exercise capacity. Typical symptoms of chronic coronary syndrome (CCS) include exertion-induced retrosternal or epigastric pain. However, less typical symptoms can also occur, including dyspnea, nausea, and even a complete lack of symptoms despite advanced CCS [1,2]. According to data from a Swedish registry, 5.2% of asymptomatic individuals had clinically significant coronary artery stenosis (≥50%) [3]. Silent cardiac ischemia occurs in 10% to 20% of cases with stable CCS [4]. Nonetheless, being oligosymptomatic does not indicate a low cardiovascular risk [4,5]. Significant stenosis of coronary arteries in athletes, especially in long-distance runners, is one of the key causes of sudden cardiac death after age 35 [6]. Diagnosing coronary artery disease can pose a clinical challenge, particularly in individuals with high exercise capacity. Chest discomfort associated with extreme levels of exertion is considered to be “physiological” and, consequently, usually does not prompt thorough cardiac diagnostics. The current literature provides limited information on the diagnostic pathway of CAD in athletes, particularly for interpretation of cardiopulmonary exercise test (CPET) and decision-making thresholds for invasive angiography in people with low risk-factor–weighted clinical likelihood (RF-CL). The present case is distinctive for 3 reasons: (1) the coexistence of supranormal exercise capacity with electrically positive CPET suggestive of ischemia, (2) coronary computed tomography angiography (CCTA) findings mimicking spontaneous coronary artery dissection in a male endurance athlete, and (3) escalation to invasive angiography despite low RF-CL guided by structured risk stratification. These elements highlight potential limitations of relying solely on functional performance metrics in athletes. The aim of this report is to present the diagnostic reasoning and therapeutic management in the case of an amateur endurance athlete who developed exertional dyspnea during a marathon run.

Case Report

INITIAL PRESENTATION:

A 50-year-old man who was a professional soldier and amateur long-distance runner with a history of hypertension (treated with nebivolol and ramipril), hyperlipidemia (atorvastatin), and hypothyroidism presented at our pulmonology outpatient clinic due to exertional dyspnea and an accompanying choking sensation that occurred during a marathon for the first time 6 months before admission. These symptoms were recurrent and were experienced after the patient had run approximately 20 km; at that point, he had to take a short rest, but it did not prevent him from completing the entire marathon.

PULMONARY WORK-UP:

None of the extensive pulmonary diagnostic investigations conducted at the outpatient clinic, including chest X-ray, spirometry, reversibility of airway obstruction, body plethysmography, and lung perfusion scan, indicated any causes of dyspnea. Consequently, the patient was referred for cardiovascular diagnostics.

CARDIAC EVALUATION:

The patient’s cardiovascular history revealed no recent symptom progression. Hypertension was well controlled with nebivolol 2.5 mg and ramipril 2.5 mg daily. Physical examination results were unremarkable. Resting electrocardiography (ECG) showed no ischemic changes, arrhythmias, or conduction abnormalities. Transthoracic echocardiography demonstrated mild left ventricular hypertrophy (interventricular septal thickness 13 mm) with preserved systolic function (ejection fraction 69%) and no regional wall motion abnormalities or diastolic dysfunction.

Given the differential diagnosis of exertional dyspnea, including exercise-induced bronchoconstriction, hypertensive response to exercise, microvascular ischemia, and obstructive coronary artery disease, the patient underwent CPET. The test showed normal exercise capacity (peak VO₂ 34 ml/min/kg, 104% of predicted; workload 224 W), appropriate chronotropic response (118% of maximum predicted heart rate), and a hypertensive peak blood pressure response (218/96 mmHg). The test was continued to near-maximal effort (RER 1.07; Borg CR RPE 8/10) without reproduction of dyspnea or chest pain. Ventilatory parameters were normal, effectively excluding pulmonary limitation or exercise-induced bronchoconstriction.

However, continuous ECG monitoring demonstrated a 1 to 2 mm ST-segment depression with T-wave changes in leads II, III, aVF, V5, and V6 at peak exercise, resolving during recovery (Figure 1A). Despite preserved functional capacity, these ischemic changes, together with an intermediate Duke Treadmill Score, raised a suspicion of myocardial ischemia and prompted further anatomical evaluation.

IMAGING:

Although the patient’s RF-CL was low (11%), the intermediate Duke Treadmill Score and electrically positive CPET findings prompted further anatomical evaluation in accordance with ESC 2024 CCS guidelines [1]. Therefore, CCTA was performed. CCTA revealed circumferential hypodense lesions (consistent with either atherosclerotic plaque or spontaneous coronary artery dissection [SCAD]) in the LAD, resulting in approximately 80% stenosis of segment 6 and approximately 90% stenosis of segment 7. Due to suspected SCAD, the patient underwent emergency coronary angiography with intravascular ultrasound (IVUS); the findings were consistent with soft, hypodense, slightly fibrotic atherosclerotic plaque obstructing 80% of the LAD lumen in segment 6 and causing a critical stenosis of segment 7 (Figure 2A). IVUS showed no intramural hematoma, and the minimal lumen area of the LAD was 2.27 mm2. Apart from these, the coronary arteries showed no other abnormalities.

MANAGEMENT:

Two drug-eluting stents were implanted into the LAD during a single procedure (Onyx TruStar 4.0/18 mm/12 atm and Onyx TruStar 4.5/22 mm/16 atm) (Figure 2B). Coronary flow was TIMI grade 3 both before and after percutaneous coronary intervention (PCI). Pharmacological therapy after PCI included rosuvastatin 30 mg, acetylsalicylic acid 75 mg, and prasugrel 10 mg. Target blood pressure was defined as 120 to 129 mmHg systolic and 70 to 79 mmHg diastolic, in accordance with current recommendations [7].

FOLLOW-UP:

Another CPET on a treadmill was conducted 5 months after the previous CPET to assess the patient’s eligibility for cardiac rehabilitation. This time, the test showed a higher exercise capacity (peak VO2 42 ml/min/kg, 127% of the predicted value, 128% of maximum predicted heart rate, with exercise duration of 9 minutes 18 seconds); there were neither exercise-limiting symptoms nor ST-segment or T-wave abnormalities indicating ischemia (Figure 1B). The formal criteria used to clear the patient for rehabilitation included the exclusion of parameters indicative of a high risk of exercise-related cardiovascular events, such as chest pain, ischemia, and arrhythmias. The intensity of training was determined based on the heart rate between the first anaerobic threshold and half the difference in heart rate between the first and second anaerobic thresholds, which corresponded to the aerobic zone. Cardiac rehabilitation included 29 telemonitored sessions over 7 weeks, during which the patient reported no symptoms and reported a subjective improvement in exercise capacity, verified via control CPET performed at the end of cardiac rehabilitation: peak VO2 improved by 5 ml/min/kg (16% of the predicted value) (Table 1) and exercise duration improved by 2 minutes. The ECG during the final CPET showed no ST-segment or T-wave abnormalities that would suggest ischemia. The patient was referred to receive further cardiological care in an outpatient setting. Qualification for possible future competitive running was postponed until 12 months after PCI, taking into account individual assessment, including another CPET.

Discussion

Based on the reported symptoms (dyspnea) and the existing CCS risk factors (dyslipidemia and hypertension), this 50-year-old male’s RF-CL of clinically significant CCS was low (11%) [1]. The potential cause of exertional dyspnea was assessed via a CPET with ECG conducted on an ergometer. During the test, the patient achieved 9.7 METs; (exercise capacity >100% of predicted) and did not develop any symptoms. Given ST-segment and T-wave abnormalities indicating ischemia of the inferior and lateral wall, the patient’s Duke Treadmill Score [8] was 2, indicating an intermediate risk of cardiovascular events. Nonetheless, due to the patient’s history of high-intensity sports and non-conventional risk factors, he was referred for CCTA, and due to suspected SCAD, coronary angiography was performed [1].

Exercise testing in individuals with average and above-average exercise capacity continues to be a challenge in everyday clinical practice. Since the purpose of an exercise stress test is to assess exercise capacity, the test should last 8 to 10 minutes [9] and be mostly based on aerobic exercise; thus, the exercise protocol must be adjusted accordingly. The commonly used Bruce protocol, and other protocols involving an increasing treadmill slope, involve a considerable component of static exercise, when the patient holds onto the railing at stages with a steep slope and high treadmill speed. The patient presented here had personalized protocols for both cycle and treadmill ergometers. He set the pace for 10 km at 7 km/h, and the exercise test was started at that pace with a level treadmill. The cycle ergometer protocol was selected in such a way as to reach the predicted workload (calculated with the Wasserman and Hansen equation adjusted for age and body weight) after 10 minutes [10]. The patient had an above-average exercise capacity, as evidenced by a peak VO2 of 104%, 127%, and 143% of the predicted value in consecutive tests. Dyspnea and a choking sensation, which first made the patient seek medical attention, had occurred only after 20 km and did not occur during CPET. The classic Canadian Cardiovascular Society angina grading scale [11], according to which class III and IV angina is reported after walking approximately 100 to 200 m, was not applicable in this case.

Another challenge was to obtain a diagnostically valid ECG tracing during running on a treadmill. In the case presented here, the adhesive electrodes were additionally secured with tape and elastic mesh dressing (Codofix) around the chest (Figure 3). It is worth remembering that exertional ECG sensitivity and specificity are 58% and 62%, respectively [12]. Nonetheless, exercise tests continue to be widely recommended in eligibility assessments for high-intensity competitive sports [13]. These tests help detect arrhythmia, channelopathy (by QTc assessment), and symptoms of ischemia during exercise that mimics actual competitions [13].

CCTA findings suggested a possible SCAD, which mostly (70%) affects women and whose etiology is not precisely known [14]. There have been reports of cases of SCAD associated with intense physical activity in various age groups, in individuals not diagnosed with atherosclerosis [15,16]. These reports indicate a need to consider SCAD while diagnosing athletes, despite the low prevalence of this condition, particularly among men. The diagnosis of atherosclerotic plaque led to the decision to implant a stent into the LAD rather than the conservative treatment recommended in SCAD [14].

Another difficulty in estimating the risk of CCS in athletes, including soldiers, is that they often follow an apparently healthy lifestyle and are not representatives of a high cardiovascular risk group (most often classified as intermediate risk [17]) according to the SCORE2 cardiovascular risk model based on conventional risk factors (eg, age, sex, systolic blood pressure, non-HDL cholesterol levels, and smoking) [18]. Individuals over 50 years of age tend to have higher rates of dyslipidemia and hypertension and a higher body weight [19]. Therefore, a holistic clinical approach should incorporate not only conventional, but also non-conventional risk factors of CCS, such as stress [17], sleep deprivation [20], inappropriate diet [21–23], and excessive physical exertion [24].

There is a noteworthy difference between highly intense competitive physical exercise and recommended moderately intense aerobic exercise of at least 150 to 300 minutes weekly. The latter is beneficial in reducing cardiovascular risk and improving exercise capacity, metabolism, immunocompetence, and mental health [25]. Moderately intense exercise is defined as maintaining 50% to 60% of the maximum heart rate, with sufficient ventilation to ensure an adequate supply of oxygen to active muscle groups and removal of the produced CO2 [26]. This level of exercise was recommended to our patient as part of his cardiac rehabilitation and resulted in an improved peak VO2, even though his physical capacity had already been shown to be above average.

Middle-age male athletes performing high-duration, high-intensity exercises are at an elevated risk of developing CAD [27]. Moreover, CAD is one of the most common causes of sudden cardiac death in athletes older than 35 [6]. The workload of long-distance runs can exceed the recommended exercise duration by as much as 10- to 15-fold [28]. Such intense exercise has been associated with metabolic and inflammatory changes, but the cause remains uncertain [6,24,29]. Hence, in well-trained endurance athletes who are familiar with their individual exercise tolerance, the occurrence of new, unexpected, or previously unexperienced symptoms such as dyspnea during usual levels of exertion should raise clinical suspicion and lead to further diagnostic evaluation, including CCTA, as such changes may indicate underlying cardiovascular disease [30].

Conclusions

This case underscores several practical implications for clinicians evaluating endurance athletes. First, preserved or supranormal exercise capacity does not exclude obstructive coronary artery disease, and mild or atypical symptoms can conceal advanced CAD. Second, risk stratification should integrate RF-CL, Duke Treadmill Score, and careful interpretation of exercise-induced ECG changes; electrically positive findings warrant anatomical imaging even when CPET performance is normal. Third, new-onset symptoms occurring at habitual levels of high-intensity exertion should prompt further evaluation, including CCTA. Finally, differentiation between spontaneous coronary artery dissection and hypodense atherosclerotic plaque is essential, as it directly determines therapeutic strategy and follow-up. Further research is needed to refine diagnostic pathways in high-capacity athletes, particularly in populations exposed to sustained physical and occupational stress.