Soo-Joong Kim

Health-Related Quality-of-Life after Percutaneous Coronary Intervention in Patients with UA/NSTEMI and STEMI: the Korean Multicenter Registry

Compared with ST elevation myocardial infarction (STEMI), long-term outcomes are known to be worse in patients with unstable angina/non-STEMI (UA/NSTEMI), which might be related to the worse health status of patients with UA/STEMI. In patients with UA/NSTEMI and STEMI underwent percutaneous coronary intervention (PCI), angina-specific and general health-related quality-of-life (HRQOL) was investigated at baseline and at 30 days after PCI. Patients with UA/NSTEMI were older and had higher frequencies in female, diabetes and hypertension. After PCI, both angina-specific and general HRQOL scores were improved, but improvement was much more frequent in angina-related HRQOL of patients with UA/NSTEMI than those with STEMI (44.2% vs 36.8%, P < 0.001). Improvement was less common in general HRQOL. At 30-days after PCI, angina-specific HRQOL of the patients with UA/NSTEMI was comparable to those with STEMI (56.1 ± 18.6 vs 56.6 ± 18.7, P = 0.521), but general HRQOL was significantly lower (0.86 ± 0.21 vs 0.89 ± 0.17, P = 0.001) after adjusting baseline characteristics (P < 0.001). In conclusion, the general health status of those with UA/NSTEMI was not good even after optimal PCI. In addition to angina-specific therapy, comprehensive supportive care would be needed to improve the general health status of acute coronary syndrome survivors.

Current statin usage for patients with acute coronary syndrome undergoing percutaneous coronary intervention: multicenter survey in Korea.

Background:

Polymorphisms of the Interferon gamma gene and coronary artery disease in the Korean population

Abundant evidence supports the hypothesis that inflammation plays an important role in the development of coronary artery disease (CAD). In this study, we investigated whether genetic polymorphisms of the Interferon gamma (IFNG) gene were associated with the number of diseased vessels in CAD patients in the Korean population. To observe the association between the IFNG gene and the number of diseased vessels, we genotyped 635 CAD patients for a single nucleotide polymorphism (SNP, rs2430561) and a microsatellite (CAn repeats, rs3138557) located in the first intron of the IFNG gene using the direct sequencing and gene scan method. The number of microsatellites was increased in the one- and two-vessel disease groups. A combined analysis of the genotype of rs2430561 and the number of microsatellites revealed that the number of diseased vessels was associated with CA12-TT and CA13-TT. Our results suggest that the IFNG gene may be one of the factors determining the extent of CAD in the Korean population. Larger collaborative studies are needed to confirm these results.

Incidence and Clinical Significance of Post-Stent OCT Findings: One Year Follow-Up Study From a Multicenter Registry

Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points (P=0.003 and P=0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization.Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points ( P =0.003 and P =0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization. # CLINICAL PERSPECTIVE {#article-title-35}

Randomized trial comparing the efficacy between different types of paclitaxel-eluting stents: The comparison of Efficacy between COroflex PLEASe ANd Taxus stent (ECO-PLEASANT) randomized controlled trial

AIMS Paclitaxel-eluting stents (PESs) have been shown to inhibit neointimal hyperplasia after percutaneous coronary intervention. Coroflex Please (B Braun, Melsungen, Germany) is a newly developed PES. We compared the clinical and angiographic efficacy of Coroflex Please with Taxus Liberte (Boston Scientific, Natick, MA) in a real-world practice. METHODS AND RESULTS We performed a prospective, open-label, randomized, controlled study that enrolled 945 patients undergoing percutaneous coronary interventions in 18 centers in Korea. The primary end point was clinically driven target vessel revascularization at 9 months. The baseline characteristics were mostly similar and comparable between 2 groups. At 9 months, the incidence of clinically driven target vessel revascularization was 14.6% for Coroflex and 6.4% for Taxus, which was significantly different (hazard ratio 2.43, 95% CI 1.50-3.94, noninferiority P value = 1.000). This is well corroborated by the difference of in-stent late loss between 2 stents (0.71 ± 0.64 mm vs 0.52 ± 0.50 mm, P < .001) by 9-month follow-up angiography (n = 415 vs 215). Among secondary clinical end points, stent thrombosis (definite and probable) for 1 year was 2.2% in Coroflex and 1.3% in Taxus (P = .317). Also, myocardial infarction for 9 months was higher in Coroflex group than that in Taxus (4.9% vs 1.6%, P = .012), which was partly contributed by the higher incidence of periprocedural myocardial infarction in Coroflex arm (2.2% vs 0.3%, P = .028). CONCLUSIONS Coroflex Please was inferior to Taxus Liberte with regard to clinical and angiographic efficacy.

Bioresorbable Vascular Scaffold Evaluation by Optical Coherence Tomography

Bioresorbable vascular scaffold (BVS) has been introduced as the latest revolution in the field of percutaneous coronary intervention (PCI), which could overcome the long-term limitations of the permanent stent implantation [1]. This device is designed to provide the temporary scaffolding of the vessel before being resorbed completely within the vessel, leaving nothing behind. It makes BVS offer a potential solution to the weakness of drug-eluting stents, which include endothelial dysfunction and hypersensitivity reactions, leading to late stent failure, and disturbance of future surgical revascularization at the same lesion [2–4].

The Use Pattern and Clinical Impact of Novel P2Y12 Receptor Antagonists for Acute Myocardial Infarction in Korea

Dual antiplatelet treatment (DAPT) with aspirin and a P2Y12 receptor antagonist is essential for patients presenting with acute coronary syndrome (ACS) irrespective of their specific percutaneous coronary intervention (PCI). Clopidogrel (Bristol-Myers Squibb/Sanofi Pharmaceuticals, Bridgewater, NJ, USA), one of the most popular P2Y12 receptor antagonists of the past decade, has reduced the risk of cardiovascular (CV) death, myocardial infarction (MI), and stroke in patients with ACS by 20–30% when added to aspirin.1) However, it has some limitations, including modest inhibition of platelet activity, delayed onset and offset of action, and inter-individual variability of pharmacodynamic responses. To overcome these drawbacks, 2 novel P2Y12 receptor antagonists, prasugrel (Eli Lilly and Company, Indianapolis, IN, USA) and ticagrelor (AstraZeneca Pharmaceuticals LP, Wilmington, DE, USA), have been developed and have demonstrated promising results. The TRial to assess Improvement in Therapeutic Outcomes by optimizing platelet inhibitioN with Prasugrel Thrombolysis In Myocardial Infarction 38 (TRITON-TIMI 38) trial found that prasugrel could reduce the composite risk of CV death, MI, or stroke in moderate-to-high-risk ACS patients undergoing PCI by 19% at the cost of higher risk of bleeding, including lifethreatening hemorrhage, compared with clopidogrel.2) Unfortunately, the use of prasugrel did not decrease CV death or overall mortality and has limitations of use in specific groups, such as elderly people (>75 years of age), patients with prior history of stroke, those with low body weight (<60 kg), or patients not concurrently receiving PCI. Ticagrelor has also shown to decrease the composite risk of CV death, MI, or stroke by 16% and the risk of CV death by 21% in ACS patients, irrespective of treatment strategy, compared with clopidogrel.3) Despite increases in both major and minor bleeding, ticagrelor did not lead to any increase in fatal bleeding. With the advent of these novel P2Y12 receptor antagonists, the combination of aspirin and prasugrel or ticagrelor instead of clopidogrel as a DAPT has been increasingly used. Contemporary guidelines recommend the use of prasugrel or ticagrelor in the setting of acute myocardial infarction (AMI).4) A few epidemiological studies from several countries have shown that the use of these novel P2Y12 receptor antagonists is rapidly increasing and has reduced the incidence of CV events or death in ACS patients compared with clopidogrel. A Danish nationwide population-based cohort study involving 28,449 patients demonstrated that the use of clopidogrel as a DAPT after AMI in 2009 had been reduced in favor of ticagrelor or prasugrel in 2012.5) The Melbourne Interventional Korean Circ J. 2017 Nov;47(6):864-867 https://doi.org/10.4070/kcj.2017.0302 pISSN 1738-5520·eISSN 1738-5555

Funtional significance of the intermediate lesion in a single coronary artery assessed by fractional flow reserve.

To the Editor, Congenital coronary artery anomalies are infrequently seen during coronary angiographic study, reportedly occurring in 0.64% to 1.3% of patients [1]. Most patients with a congenital coronary artery anomaly are asymptomatic; in rare cases, they may present with chest pain and have myocardial ischemia or other life-threatening conditions. We present a patient with the right coronary artery (RCA) originating from the terminal branch of the left circumflex (LCx) artery who presented with chest pain and was found to have a moderate stenotic lesion in the distal LCx artery. Fractional flow reserve (FFR) allowed us to evaluate this moderate stenotic lesion in a single coronary artery, and to treat with medical therapy only. A 63-year-old man was admitted to the cardiology unit with atypical chest pain. He had hypertension as coronary heart disease risk factor. His vital signs were stable, and physical examination showed no abnormalities. A resting electrocardiogram demonstrated a convex-shaped ST-segment elevation in the precordial lead without reciprocal change. Laboratory findings including cardiac markers showed no abnormalities. Echocardiography revealed normal left ventricular morphology, no regional wall motion abnormality, and a diastolic dysfunction of relaxation abnormality. The patient underwent coronary computed tomographic (CT) angiography. It demonstrated the presence of a single coronary artery with the LCx artery continuing in the course of the RCA and minimal possibility of chronic total occlusion (CTO) of the RCA ostium with a collateral supply from the LCx artery (Fig. 1). It also showed 60% diameter stenosis in the distal LCx artery (Fig. 1). Figure 1 Coronary computed tomography (CT) angiography findings. (A, B) Volume rendering CT imaging and (C) multiplanar reformation image showed a single coronary artery in which the right coronary artery (RCA) originated from a branch of the left circumflex (LCx) ... To differentiate single coronary artery from CTO of the RCA ostium and confirm the degree of stenosis in the distal LCx artery, we performed coronary angiography. Selective left coronary angiography displayed normal origin and course of the left main, LCx, and left anterior descending arteries. The LCx artery did not terminate after reaching the crux; giving rise to the posterior descending branch, it coursed in the right atrioventricular groove as if it were the RCA and ended when it reached the right sinus of Valsalva (Fig. 2A). There was a stenosis of 60% diameter in the distal part of the LCx proper where the RCA arose (Fig. 2B). Attempts to engage the right coronary catheter into the RCA ostium were futile, and aortography obtained in the left anterior-oblique projection displayed the absence of the ostium of the RCA in the right sinus of Valsalva (Fig. 2C). To decide the functional significance of the stenosis in the distal LCx artery, we performed an FFR study with a pressure wire and found that there was no critical functional stenosis (FFR, 0.9) (Fig. 2D). The patient was discharged with medications of aspirin, statin, nitrate, and β blocker and free from chest pain. Figure 2 (A) The single coronary artery visualized in the caudal angulation. (B) The left anterior oblique caudal view of selective left coronary angiography showed a stenosis of 60% in the distal left circumflex (LCx) proper artery (arrow)

Unexpected development of acute abdominal aortic thrombosis during percutaneous coronary intervention.

To the Editor, Acute aortic occlusion by a thrombus is an uncommon vascular emergency during percutaneous coronary intervention (PCI), which may lead to shock and death. We report on a patient who experienced acute thrombosis at the aortoiliac bifurcation and was treated by aspirating a thrombus and implanting a stent in the aorta. An 82-year-old female with a history of hypertension, diabetes, atrial fibrillation, and cerebral infarction was referred to the Cardiology Department due to chest discomfort and elevated cardiac biomarkers (creatinine kinase/creatinine kinase-MB, 33/7.0 IU/L; troponin I, 0.18 ng/mL) before a colorectal fistula operation. Coronary angiography was performed under the impression of a non-ST elevation myocardial infarction, which clearly showed a high-grade stenosis in the mid-portion of the left anterior descending (LAD) artery with minimal luminal area < 2 mm2 on the intravascular ultrasound evaluation (Fig. 1). Unfractionated heparin (70 units/kg) was administered initially. Then, activated clotting time was monitored and maintained at 200 to 300 seconds by an additional injection of heparin during PCI. When a guiding catheter (JL 7 Fr) was engaged into the LAD artery, central blood pressure decreased and unusual flat pattern pressure curves appeared, together with dizziness (Fig. 2A). We retracted the guiding catheter and performed aortography through the contralateral femoral artery. No aortic dissection was detected in the ascending or descending aorta. However, aortography showed a huge, lumen-occluding thrombi at the level of aortoiliac bifurcation (Fig. 2B). We initially infused 200,000 U tissue plasminogen activator into the aortic bifurcation through the guiding catheter and manually aspirated using a 9-Fr long sheath, but huge thrombi remained in the aortoiliac bifurcation, and an angiogram showed no pathological evidence of abdominal aorta bifurcation such as severe occlusive disease, aortic dissection, or abdominal aortic aneurysm (Fig. 2C). The aspirated material was a 6-cm black-colored thrombus (Fig. 2D). We inserted a stent in the aorta and two self-expandable aortic stents (10 mm × 6 cm at the left side and 10 mm × 8 cm at the right side (Zilver, Cook Medical, Bloomington, IN, USA) were implanted at the aortoiliac bifurcation. After deployment of the stents, additional ballooning (8 mm × 4 cm, Rider, Cook Medical) was performed. A final angiogram showed a good result (Fig. 3). The patient recovered well after stent implantation, with blood pressure of 110/70 mmHg. She underwent PCI successfully at the mid-LAD artery and was discharged uneventfully 7 days later. Figure 1 Coronary angiogram and intravascular ultrasound examination showed significant stenosis in the mid left anterior descending artery. Figure 2 (A) Blood pressure monitoring connected to a femoral sheath showed decreased aortic pressure, followed by appearance of unusual pressure curves of a flat-curved pattern. (B) Aortogram showed a huge and lumen-occluding thrombus at the aortoiliac bifurcation. ... Figure 3 (A, B) Successful insertion of an aortic stent for coverage of thrombi in the abdominal aortic bifurcation. Acute thrombotic occlusion of the aorta during PCI is a rare event, resulting in disastrous consequences unless an early diagnosis is made and appropriate management initiated [1]. The cause of an occlusion is a saddle embolus at the aortoiliac bifurcation or acute in situ thrombosis on a background of severe occlusive disease, aortic dissection, acute thrombosis of an abdominal aortic aneurysm, vasculitis, hypercoagulability, or aortic trauma [2]. Other uncommon causes include a fungal infection, acute thrombosis of abdominal aortic stent-graft in heparin-induced thrombocytopenia, or chemotherapy-related thrombosis [3,4,5]. Compared with other causes of acute aortic occlusion, acute thrombosis at the aortoiliac bifurcation during PCI is extremely rare. As a prerequisite check before guiding catheter engagement, we assessed the activated partial thromboplastin time and flushed the femoral sheath with saline, but no abnormal findings were detected. In this case, no abnormal findings in the aorta were observed, including aneurysm, dissection, or trauma. We also examined protein C and S activity, erythrocyte sedimentation rate, C-reactive protein, complement 3 and 4, and antineutrophil cytoplasmic antibody to evaluate hypercoagulability and vasculitis, but no abnormal results were found. No fungal infection was identified. Atrial fibrillation was another possible contributor to embolic occlusion but there was no thrombus in the left atrial appendage or left ventricle on echocardiography. Therefore, we finally suspected a saddle embolus originating from the femoral sheath and an in situ thrombosis at the aortoiliac bifurcation as a possible cause of this PCI-related aortic complication. Anticoagulation should be initiated immediately once the diagnosis of acute thrombotic occlusion in aorta is made, and early revascularization should be the goal. Possible revascularization approaches include thromboembolectomy, aortic reconstruction, anatomic or extra-anatomic bypass, and thrombolysis. The choice of approach depends on the etiology, anatomy, and patient factors. Surgical thrombectomy has frequently been used for treatment of an acute aortic occlusion. However, recent advances in endovascular techniques could decrease the high mortality rate associated with surgical treatment of this disease and warrants consideration as a treatment option. In this case, we decided on endovascular treatment for revascularization with thrombolysis, thrombus aspiration, and stent implantation using a contralateral approach. In conclusion, acute thrombosis can occur at the aortoiliac bifurcation during PCI. Therefore, operators should pay attention to the development of aortic complications upon encountering an abnormal central blood pressure pattern and consider an appropriate treatment method-including an endovascular approach-for acute aortic thrombosis.

A case of primary aldosteronism presenting as non-ST elevation myocardial infarction.

To the Editor, Primary aldosteronism (PA) is associated with several cardiovascular diseases. Postulated mechanisms include inappropriate volume retention, suppression of endothelial function, and target organ inflammation and fibrosis. While heart failure in conjunction with arrhythmias is the most common cardiovascular complication in PA, few cases of coronary artery disease (CAD) in concurrence with PA have been reported [1-3]. Here, we propose a possible mechanism for CAD developing in PA based on a case of PA presenting as non-ST elevation myocardial infarction (NSTEMI) in the absence of heart failure or other comorbidities in a relatively young Korean male. To our knowledge, this is the first report of PA presenting with NSTEMI. A 43-year-old male with a 10-year history of treatment-resistant hypertension presented to the cardiology outpatient clinic with stabbing chest pain in the retrosternal area. The pain began at rest and lasted for a few seconds to a few minutes. To treat his hypertension, he was taking carvedilol 25 mg, telmisartan 80 mg, and spironolactone 25 mg. He had a 20 pack-years smoking history, but no family history of cardiovascular disease. He was admitted for further investigations. On admission, his blood pressure was 130/80 mmHg, pulse 66 per minute, body temperature 36℃, respiration rate 20 per minute, and body mass index 23.0 kg/m2. The initial laboratory testing yielded serum sodium 144 mmol/L, potassium 2.7 mmol/L, chloride 101 mmol/L, blood urea nitrogen 12 mg/dL, creatinine 0.9 mg/dL, troponin-I 0.16 ng/mL, creatine kinase 78 U/L, high-sensitivity C-reactive protein (hs-CRP) 1.81 mg/L, and creatinine kinase-MB 1.9 ng/mL. The lipid profile, liver function tests, and complete blood count with differential were all within normal limits. The chest X-ray was unremarkable and the initial electrocardiograph (ECG) showed a prominent U wave in all precordial leads and T wave inversion in V3 to 5. Echocardiography revealed a normal ejection fraction (70%) with no valvular abnormality. The right and left carotid intima-media thickness (IMT) was 0.6 and 0.5 mm, respectively, without visible plaque. The brachial artery flow-mediated dilation (FMD), pulse wave velocity (PWV), ankle-brachial index (ABI) bilaterally, and cardioankle vascular index (CAVI) bilaterally were all normal. Based on these findings, NSTEMI was diagnosed and followed by coronary angiography with successful percutaneous coronary intervention (PCI) with a drug-eluting stent at the mid-left anterior descending artery (Fig. 1). Figure 1 Coronary angiography demonstrating 75% diameter stenosis of the mid-left anterior descending artery. After PCI, his serum potassium and blood pressure remained uncorrected despite oral potassium supplementation and three antihypertensive medications. In light of his uncorrected electrolyte and blood pressure, additional endocrinological tests were performed. His thyroid-stimulating hormone level was 2.46 µU/mL, free T4 1.36 ng/dL, T3 143 ng/dL, 24-hour urine free cortisol 71 µg/day, urine vanillylmandelic acid 2.0 mg/day, urine norepinephrine 118.2 µg/day, urine epinephrine 11 ng/day, urine metanephrine 0.4 mg/day plasma norepinephrine 0.28 ng/mL, plasma epinephrine 0.04 ng/mL, plasma adrenocorticotropic hormone 65.2 pg/mL at 8:00 AM and 22.8 pg/mL at 4:00 PM, plasma cortisol 21.2 µg/dL (585.12 nmol/L) at 8:00 AM, 9.4 µg/dL (259.44 nmol/L) at 4:00 PM, and 15.6 µg/dL (430.56 nmol/L) at midnight, plasma aldosterone 1,080.3 pmol/L (cutoff value > 450 pmol/L), plasma renin activity (PRA) 0.1 ng/mL/hr, and aldosterone-renin ratio 10,803 pmol/L:ng/mL/hr (cutoff value > 750 pmol/L:ng/mL/hr). To avoid misinterpretation of the plasma cortisol level during a stressful condition (i.e., NSTEMI), we checked the serum cortisol level several times during the following 6 months and confirmed a consistently elevated level. Suspecting PA, abdominal computed tomography revealed a 1.4 × 1.2-cm mass at the right adrenal gland (Fig. 2A). After discontinuing all antihypertensive drugs, he underwent the furosemide loading test, which showed no response. Based on the high 24-hour urine free cortisol level, an overnight dexamethasone suppression test (DST) was done. After a 1-mg dose DST, the plasma cortisol level was 2.2 µg/dL. Subsequently, a low-dose DST was performed, but the result was negative. Hence, we could rule out Cushing syndrome. Figure 2 (A) Abdominal computed tomography showing an adrenal adenoma of the right adrenal gland, medial limb. (B) Histopathology confirming adrenocortical adenoma (light microscopy, H&E, × 200). The adrenal adenoma was removed laparoscopically; the specimen showed a cortical adenoma with primarily cortical hypertrophy mixed with regions of partial cortical atrophy, suggesting autonomous cortisol secretion (Fig. 2B). Postoperatively, his blood pressure, serum potassium level, and ECG normalized. The chronically elevated serum aldosterone level in patients with PA makes them susceptible to a wide spectrum of cardiovascular diseases, from arrhythmias to congestive heart failure and CAD. The relatively high incidence of heart failure in conjunction with arrhythmias in patients with PA can be explained by left ventricular hypertrophy due to hypertension, hypokalemia, and cardiac fibrosis due to aldosterone excess [1-3]. Although many have hypothesized that aldosterone plays a role in the development of CAD, the number of cases of PA occurring in concurrence with CAD remains very small, especially in Asian populations. Although Nakajima et al. [4] reported a myocardial infarction occurring in PA and Nishimura et al. [2] stable angina in PA, these patients were elderly, leaving room for discussion as to whether age along with other comorbidities associated with senility contributed to the outcome [1]. The reasons for the obvious discrepancy in the incidence of heart failure and CAD have never been explored nor has the exact mechanism underlying the development of CAD in PA been established. This case is interesting in terms of the pathophysiological role of aldosterone in the development of NSTEMI in a relatively young patient with no risk factors for CAD other than smoking. It is also notable that despite the long history of treatment-resistant hypertension, there were no signs of endothelial dysfunction or arterial stiffness, evident by the normal FMD, PWV, ABI, CAVI, hs-CRP, and carotid IMT. The atherosclerotic lesions were limited to the coronary artery. In addition, the fact that his NSTEMI was diagnosed before the diagnosis of PA makes this case unique. It appears that the lack of symptoms owing to hypokalemia, muscle weakness, and constipation delayed the detection of the PA. We would like to highlight that this NSTEMI occurred in the absence of left ventricular dysfunction, suggesting that a separate mechanism exists for the development of CAD. Although we were not able to prove it, after reviewing various studies, we suggest the autonomous secretion of cortisol in association with PA as the culprit. Recent studies support the strong correlation between the autonomous secretion of cortisol and the increase in cardiovascular events [4]. This patient had an elevated midnight cortisol, an initial 24-hour urine cortisol > 50 µg/day, and a plasma cortisol level after 1-mg DST > 2.0 µg/dL; all suggest subclinical hypercortisolism. Hypercortisolism is associated with the decreased production of vasodilators, such as nitric oxide (NO), in coronary artery endothelial cells, and this might lead to the development of CAD. Rogers et al. [5] suggested the following as the mechanism of NO synthesis downregulation: 1) decreased endothelial NO synthase (eNOS) mRNA expression, 2) increased degradation of eNOS mRNA, 3) decreased eNOS protein stability, and 4) decreased agonist-mediated intracellular calcium mobilization. Such changes inevitably lead to an increased risk of CAD developing. Although we did not demonstrate a relationship between hypercortisolism and NO production in this case, it is safe to say that this case, at least, corroborates the role of cortisol in the development of coronary events. Another possible mechanism might be that chronic aldosterone excess alters the normal immune response system by activating proinflammatory mediators such as intercellular adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-1, plasminogen activator inhibitor-1, and matrix metalloproteinases, thereby setting a proinflammatory vascular phenotype and plaque vulnerability [3]. This inflammatory and endothelial dysfunction might be responsible for the development of CAD in PA patients. In conclusion, measuring serum cortisol level might help to predict CAD development in patients with PA. In addition, in CAD patients without typical risk factors, secondary endocrine causes should be suspected.