Hee Jeoung Yoon

The Association Between Current Helicobacter pylori Infection and Coronary Artery Disease

Background The role of Helicobacter pylori (H. pylori) in the pathogenesis of coronary artery disease (CAD) is still controversial, and the relation between current H. pylori infection and CAD has not been fully examined. This study evaluated the relation between H. pylori infection as confirmed by gastroduodenoscopic biopsy and CAD. Methods We determined the presence of H. pylori infections, via gastroduodenoscopy, in 88 patients of the normal coronary angiographic group and also in 175 patients of the CAD group, and the latter patients had more than 50% coronary stenosis angiographically demonstrated. We excluded those patients with a history of previous H. pylori eradication and/or malignancy. A small piece of tissue from the antrum, which was obtained by gastroduodenoscopic biopsy, was stained by Warthin-starry silver stain. We defined a negative staining result that there was no stained tissue in the sample and the stained tissue was also positive for H. pylori infection. Results There was no significant difference, except for gender, age, smoking and high density lipoprotein cholesterol (HDL-c), of the demographic and laboratory characteristics between the groups. Twenty seven (30.7%) patients of the normal control group and 71 (40.6%) patients of the CAD group were positive of H. pylori infection, yet there was no statistical difference. We angiographically followed up the 80 patients of the CAD group who were treated by percutaneous coronary intervention (PCI) at 6 to 9 months after their primary intervention. Twenty two (37.9%) of the 58 patients of the H. pylori negative group and 10 (45.5%) of the 22 patients of the H. pylori positive group were treated with reintervention, but reintervention was also not significantly different between the group with H. pylori infection and the group without the infection. Conclusions These data indicated that H. pylori infection had a modest influence on CAD and progressive atheroma, but the showed a tendency to increase. Further studies are needed to evaluate the relationship between H. pylori infection and CAD.

Adenosine Tc-99m tetrofosmin SPECT in differentiation of ischemic from nonischemic cardiomyopathy in patients with LV systolic dysfunction.

Background: The noninvasive differentiation of ischemic from nonischemic cardiomyopathy is clinically important. However, whether adenosine Tc-99m tetrofosmin SPECT can offer clear and accurate information was not known. The aim of this study is to investigate the usefulness of adenosine Tc-99m tetrofosmin SPECT in differentiation of ischemic from nonischemic etiology in patients with mild to severe LV systolic dysfunction and to compare the relationship between patients with mild LV systolic dysfunction and those with severe LV systolic dysfunction. Methods: Seventy-five patients with chronic heart failure (LV ejection fraction ≤50%) underwent adenosine Tc-99m tetrofosmin SPECT and coronary angiography to identify ischemia. The patients were divided into 2 groups based on the result of ejection fraction (EF); group I (44 patients) had mild LV dysfunction, LVEF >35%, group II (31 patients) had severe LV dysfunction, LVEF ≤35%. As the result of SPECT, percent abnormal myocardium was categorized into 3 groups: small defect, <10%; medium defect 10% to 20%; and large defects, ≥20%. Myocardial ischemia was defined by ≥70% stenosis in at least one vessel by coronary angiography. Results: In group I, 4 (30.8%) of 13 patients with small defects, 1 (25.0%) of 5 patients with a medium defect, and 22 (84.6%) of 26 patients with large defects demonstrated myocardial ischemia documented by coronary angiography. The relationship between the extent of the SPECT defect and myocardial ischemia was statistically significant in the group I population (P < 0.001). However, in group II, 1 (33.3%) of 3 patients with small defect, 3 (33.3%) of 9 patients with medium defects, and 7 (36.8%) of 19 patients with large defects demonstrated myocardial ischemia confirmed by coronary angiography. There was no statistical relationship between the extent of the SPECT defect and myocardial ischemia in group II. Conclusions: Adenosine Tc-99m tetrofosmin SPECT is a useful modality to differentiate ischemic from nonischemic etiology in patients with mild LV systolic dysfunction. However, other noninvasive approaches other this SPECT may be considered for confirming the etiology in patients with severe LV systolic dysfunction.

Effects of Combined Therapy with Ezetimibe Plus Simvastatin After Drug-Eluting Stent Implantation in a Porcine Coronary Restenosis Model

The aim of this study was to examine the anti-proliferative and anti-inflammatory effects of ezetimibe/simvastatin (E/S) after drug-eluting stent (DES) implantation in a porcine coronary restenosis model. Pigs were randomized into two groups in which the coronary arteries (23 pigs) had DES. Stents were deployed with oversizing (stent/artery ratio 1.3:1) in porcine coronary arteries. Fifteen pigs were taken 10/20 mg of E/S and eight pigs were not taken E/S. Histopathologic analysis was assessed at 28 days after stenting. In neointima, most inflammatory cells were lymphohistiocytes. Lymphohistiocyte count was not different between two groups (337±227 vs. 443±366 cells, P=0.292), but neointima area was significantly smaller (1.00±0.49 mm2 vs. 1.69±0.98 mm2, P=0.021) and percent area stenosis was significantly lower (23.3±10% vs. 39±19%, P=0.007) in E/S group compared with control group. There were no significant differences in fibrin score (1.99±0.79 vs. 1.81±0.88, P=0.49), endothelial score (1.75±0.66 vs. 1.80±0.59, P=0.79), and the percent of endothelium covered lumen (43±21% vs. 45±21%, P=0.84) between E/S group and control group. Combined therapy with ezetimibe and simvastatin inhibits neointimal hyperplasia, but does not inhibit inflammatory infiltration and arterial healing after DES implantation in a porcine coronary restenosis model.

Type 4 dual left anterior descending coronary artery

To the Editor, Anomalies of and variations in the coronary arteries are important in pathophysiology and the treatment of cardiovascular diseases. The left anterior descending (LAD) coronary artery has the most constant origin, course, and distribution in the human heart; anomalies are rare. Dual LAD was first reported and classified into four types by Spindola-Franco et al. [1] Among these four types, a type 4 anomaly comprises two LADs: a short LAD that originates from the left coronary arteries, terminates in the middle of the anterior interventricular sulcus (AIVS), and does not reach the apex, and a long LAD that originates from the right coronary artery (RCA) transverse to the right ventricular infundibulum, enters the AIVS, and courses to the apex. Type 4 dual LAD is one of the rarest of coronary anomalies. Here, we report a rare case of dual LAD arising from the left and right coronary arteries with superimposed atherosclerotic coronary artery disease (CAD). A 69-year-old man presented to our cardiology department with chest pain, which was aggravated by fast walking and relieved by rest. His medical history included surgery for spinal stenosis, prolonged steroid use, and iatrogenic Cushing syndrome. He had a 60-pack-year history of smoking, but had quit 3 years earlier. No specific findings were obtained from a physical examination and laboratory testing other than serum hepatitis B virus surface antigen positivity. A normal chest X-ray was obtained. An electrocardiogram showed a normal sinus rhythm without any remarkable abnormalities. Transthoracic echocardiography revealed suspicious hypokinesia at the posterolateral wall with aortic valve sclerosis and an ejection fraction of 57%. The patient also underwent cardiac single-photon emission computed tomography (SPECT), which showed an irreversible photon deficiency in the septum and reversible photon deficiency in the anterior wall and apex. To evaluate the patient’s chest pain and rule out CAD, we performed coronary angiography using the standard right femoral Judkin technique. A left coronary angiogram revealed a short LAD and left circumflex artery (LCX). The LAD was not visualized near the apicoseptal region of the left ventricle. The mid and distal portions of the LAD were avascular and free of collateral circulation. The LAD traveled normally and terminated after the small second septal and diagonal branches (Fig. 1A). A selective right coronary angiogram revealed an anomalous branch that originated from the proximal RCA and coursed very closely with the short LAD, which originated from the left main artery in the AIVS and terminated at the apex (Fig. 1B). We interpreted this angiographic finding as the LAD, supplied by both the left main coronary artery and RCA. Significant atherosclerotic stenosis was detected in the proximal and middle portions of the LCX (Fig. 2A). On-site percutaneous coronary intervention (PCI) was performed for the LCX with a 3.5 × 24.0-mm Pico stent for the proximal lesion and a 3.0 × 30.0-mm Pico stent for the middle lesion (Fig. 2B). The patient was discharged 1 day after PCI without complications. Figure 1. A coronary angiogram showing the left anterior descending (LAD). (A) A short LAD (arrow) was found to terminate in the middle of the anterior interventricular sulcus after small second septal and diagonal branches. (B) An anomalous branch from the proximal ... Figure 2. A coronary angiogram showing the left circumflex artery (LCX). (A) Critical stenosis was seen in the proximal and middle LCX (arrows). (B) Successful coronary intervention for the LCX was performed using two Pico stents and balloon angioplasty. The broad application of coronary angiography has revealed many anomalies of the coronary arteries that vary in number, origin, course, distribution, and termination point. In 1983, Spindola-Franco et al. [1] reported 23 cases of dual LAD and classified the anomaly into four subtypes according to the origin and course of the long LAD, as follows. Type 1: the short LAD runs in the AIVS and is generally the source of all major proximal septal perforators. The long LAD also runs in the AIVS, descending on the left ventricular side of the AIVS and reentering the distal AIVS to reach the apex. Type 2: the short LAD is the same as in type 1, but the long LAD descends over the right ventricular side before reentering the AIVS. Type 3: the short LAD is consistent with that in types 1 and 2. The long LAD travels intramyocardially in the ventricular septum. Type 4: high in the AIVS, a very short vessel is formed by the LAD proper and the short LAD. The major septal perforators and diagonal branches originate from this vessel. The long LAD is from the RCA. Type 1 to 3 anomalies arise separately from the proximal part of the LAD and are divided into two left coronary arteries. In a type 4 LAD, the LAD is supplied by the LAD proper and the RCA. It is extremely rare among the four types; only a few cases have been reported worldwide to date [1-5]. Kunimoto et al. [2] reported a case of type 4 dual LAD confirmed by both multidetector-row computed tomography and coronary angiography, while Kosar [4] reported a type 4 dual LAD found incidentally in a patient with LCX stenosis. In our patient, the long LAD originated from the RCA and coursed very closely with a short LAD originating from the left main artery in the AIVS that terminated at the apex. Therefore, this anomaly was classified as a type IV dual LAD. Dual LAD is benign in nature and usually asymptomatic. However, when atherosclerotic CAD is present, it is difficult to differentiate major stenosis or occlusion of the mid or distal portion of the LAD from this anomaly. Whether or not this anomaly can precipitate CAD has not been established. The angiographic evaluation of coronary artery anomalies is crucial for both coronary artery intervention and surgery involving the coronary arteries [1-5]. In patients with suspected acute coronary syndrome superimposed by coronary artery anomalies, a mismatch may occur between the results of noninvasive studies of the involved vessel (e.g., echocardiography or cardiac SPECT) and those of coronary angiography. Knowledge of these anomalies would help clinicians locate the correct culprit lesion and prevent erroneous decisions. Spindola-Franco et al. [1] described a patient with type 4 dual LAD and an acute ventricular septal defect in the apical portion of the interventricular septum. Occlusion of the RCA and severe disease of the long LAD explained the apical septal rupture in the presence of a patent LAD proper and a normal, short LAD [1]. In conclusion, we treated a patient with type 4 dual LAD and an atherosclerotic lesion in the LCX. Being alert to this coronary artery anomaly will help clinicians to diagnose and manage patients properly. To our knowledge, this is the first such case in Korea.

Complete fracture of sirolimus-eluting stent in a saphenous vein graft to left anterior descending artery.

Coronary stent fractures have been suggested as a potential new mechanism of restenosis. The mechanical properties of stents were designed not only to prevent vessel recoil, but also to resist the mechanical stress of vessel movement over millions of cardiac cycles. We present a case in which mechanical stress may have contributed to the fracture of a stent implanted in a saphenous vein graft (SVG) to the left coronary artery. The patient was admitted due to chest pain 2 years after receiving a coronary artery bypass graft. A coronary angiography revealed the culprit vessel to be the SVG to the left coronary artery. The graft was stenosed and was stented with a sirolimus-eluting stent. A 6-month follow-up coronary angiography revealed 80% in-stent restenosis with stent fracture. We re-intervened by balloon angioplasty. This is the first report of sirolimus-eluting stent fracture combined with restenosis of SVG in Korea.