Direct percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is now established as a standard therapy for older patients. However, experience with PCI in very young adults with AMI has been limited. In this report we retrospectively evaluated the effectiveness of PCI for very young adults with AMI and estimated their clinical characteristics and outcome. Of the 502 patients with AMI, 5 were 35 years old or younger (1.0%) during a period of 4 years (2000-2004). We assessed the utility of PCI in these five consecutive patients under the age of 35 presenting with a first AMI. Five AMI patients, ranging in age from 20 to 34 years (median, 27 ± 5 years) underwent direct PCI for the culprit lesions. The lesions targeted for PCI were located in the left anterior descending artery in 3 patients and in the right coronary artery in 2 patients. One patient had a past history of Kawasaki disease (KD). In all of the patients, PCI were angiographically effective at the acute phase without complication. In hospital course, a subacute stent thrombosis occurred in one patient. Follow-up angiograms performed 6 months after the procedure revealed no restenosis, but identified a new coronary aneurysm in one patient with a past history of KD and a regressed giant coronary aneurysm probably due to atypical KD in another patient, which were confirmed by intravascular ultrasound. There was one death ascribed to heart failure 8 months after the initial PCI. The findings of this report suggest that PCI for very young adults with AMI can be safe and effective in the short-term.
We compared the effects of ticlopidine and cilostazol on the prevention of subacute stent thrombosis (SAT) in acute myocardial infarction (AMI) patients with stenting. We also analyzed the cause of the difference by measuring platelet aggregation activity. Consecutive patients who underwent successful stenting for AMI between March 2001 and March 2004 were analyzed. In addition to aspirin (100 mg/day), cilostazol (200 mg/day) was administered to 99 cases between March 2001 and May 2002 and ticlopidine (200 mg/day) was administered to 85 cases between June 2002 and February 2004. The incidence of SAT within four weeks after stenting was analyzed. Thirty-eight AMI patients were randomized and their platelet aggregation activity was measured using a laser-scattered aggregometer (18 cases in the cilostazol group and 20 cases in the ticlopidine group). SAT did not occur in the ticlopidine group while 5 cases (5.1%) of SAT occurred in the cilostazol group (P < 0.05). The inhibitory activity of cilostazol for ADP-induced platelet aggregation was lower than that of ticlopidine (P < 0.05). Cilostazol with aspirin after stenting in AMI patients showed more frequent SAT than ticlopidine with aspirin. One of the causes for this difference was speculated to be the weaker inhibitory activity of cilostazol for ADP-induced platelet aggregation.
Although several investigations have reported that stent implantation is an option for the treatment of vasospastic angina (VSA) that is resistant to medical treatment, we are concerned about the occurrence of new stent-edge spasms after stenting. The purpose of this study was to determine the incidence of new stent-edge spasms after stenting. Twenty-seven patients with VSA and 23 patients without VSA were enrolled. About 6 months after stent implantaion, a spasm provocation test was performed by intracoronary infusion of acetylcholine or ergonovine in 26 patients with VSA and all patients without VSA, and the induced stent-edge spasms were classified as either moderate (stent-edge spasm > 75% and < 95% reduction in coronary artery diameter) or severe (stent-edge spasm > 95% reduction in coronary artery diameter). In one patient with VSA, stent-edge spasm and acute thrombosis occurred several hours after stent implantation. The remaining 26 patients with VSA had no complications during or after stent implantation. However, during the chronic phase, severe stent-edge spasm was provoked in 5 patients with VSA (19.2%) and in 2 patients without VSA (8.7%). Moderate stent-edge spasm was provoked in 5 patients with VSA (19.2%) and 5 patients without VSA (21.7%). The results suggest new onset stent-edge spasm in patients either with or without VSA should not be neglected.
While coronary artery dissection caused by a guiding catheter, which is one of the most commonly occurring complications during diagnostic cardiac catheterization or coronary intervention, has various forms, extensive antegrade and retrograde dissections of the right coronary artery (RCA) are rarely observed during these procedures. Within the last three years, we retrospectively reviewed our experience with 12,600 consecutive patients who underwent either diagnostic cardiac catheterization or coronary angioplasty, and found that 17 (0.14%) of the patients displayed extensive antegrade and retrograde RCA dissection. The antegrade dissection always propagated to the distal RCA either on bifurcation of the posterior descending artery and posterolateral artery (PLA) or to the proximal PLA. The retrograde dissection was always observed close to the ostium of the RCA or extending to the ostium of the RCA. TIMI-0 flow in the RCA was immediately observed in all the patients. Chest pain associated with an electrocardiogram showing ST-segment elevation was soon observed in most of the patients. The true lumen could be entered successfully using a single wire in 8 of 17 patients. However, a double-wire technique was required for 7 patients. This technique involved first advancing a wire along to the false lumen and then pulling back the guiding catheter away from the ostium of the RCA for a few millimeters followed by anchoring with the wire. Another wire was then gently inserted into the true lumen from the dissection entrance point, which was located near or at the ostium of RCA, and carefully advanced to the distal RCA. Coronary stenting was successfully deployed in 15 patients. However, the procedure failed in 2 patients. Furthermore, this complication caused 7 patients to have acute myocardial infarctions, 2 patients to develop atrial fibrillation, and 1 to die from ischemic enterocolitis due to cardiac embolism after 7 months of follow-up. In conclusion, with an increase in experience, we now better understand this complication. However, this complication, which is a formidable challenge for coronary intervention, may be a life-threatening complication, and patients with this complication may face the potential risk of a nonfatal myocardial infarction, or even a long-term fatal outcome in the long-term. Accordingly, it is important to learn how to promptly manage this complication.
The effects of the addition of a nitric oxide (NO) donor to the cardioplegic solution on reperfusion injury and lipid peroxidation (LPO) in coronary artery bypass grafting (CABG) are not known. Therefore, this work was conducted to determine the possible effects of nitroglycerin on LPO and reperfusion injury as a result of CABG. A prospective double-blind, placebo-controlled study was conducted in 30 consecutive patients with coronary artery disease who underwent CABG with cardiopulmonary bypass. The patients were randomly assigned to receive 3 μg/kg of nitroglycerin added to the cardioplegic solution (NTG group) or 3 μg/kg of placebo added to the cardioplegic solution (placebo group). MDA increased significantly in the placebo group compared to the NTG group during the ischemic (P < 0.01) and reperfusion periods (P < 0.01). The level of troponin I decreased significantly in the NTG group compared to the placebo group during the ischemic and reperfusion periods (P < 0.001). The level of NO increased significantly in the NTG group compared to the placebo group during the ischemic and reperfusion periods (P < 0.01). LPO was increased in response to CPB during CABG, together with simultaneous decreases in serum nitric oxide levels, whereas LPO was significantly decreased in response to CPB with nitroglycerin, together with simultaneous increases in the levels of serum nitric oxide.
The aim of the present study was to establish an evidence-based effective prediction model for improving the accuracy and priority for undertaking coronary angiography. The sample population consisted of 2002 coronary angiography patients. Our data were taken from claim forms provided by the Taiwanese Bureau of National Health Insurance. The results were tested using chi-square automatic interaction detection to establish a prediction model using coronary risk factors. We found significant variation across homogeneous groups, with the probabilities of developing coronary heart disease (CHD) varying according to risk factors such as sex, hypertension, diabetes, age, and physical inactivity. The study also explored the influence of interactions among patient characteristics. The sensitivity, specificity, and positive predictive value of our study were 92.0%, 35.4%, and 76.5% respectively, indicating the diagnostic accuracy of the model is at least as high as the treadmill exercise test. The results suggest that the accuracy of a decision concerning the performance of cardiac angiography can be significantly enhanced by an evidence-based effective prediction model that takes interactions between risk factors into account. This model also helps to priortize patients waiting to undergo coronary angiography.
There is increasing evidence that peripheral pulse pressure measured at the brachial artery is a good predictor of coronary heart disease. However, the relation between pulse pressure and angiographically demonstrated coronary artery stenosis has not been fully elucidated. We designed the present study to investigate the association of the various components of blood pressure, such as systolic pressure, diastolic pressure, and pulse pressure of both peripheral and central arteries with angiographically determined coronary artery stenosis. Levels of aortic systolic pressure, aortic diastolic pressure, aortic pulse pressure, peripheral systolic pressure, peripheral diastolic pressure, and peripheral pulse pressure were determined in 323 patients who underwent diagnostic coronary angiography. Of these 323 patients, 215 patients had significant organic coronary artery stenosis. Aortic pulse pressure was significantly higher in patients with coronary artery stenosis (P = 0.0050). Aortic diastolic pressure was lower in patients with coronary artery stenosis (marginally significant, P = 0.0462). However, no statistically significant difference was observed between other blood pressure components and coronary artery stenosis. Multivariate analyses showed that aortic pulse pressure was associated with coronary artery stenosis independently of aortic diastolic pressure. Moreover, aortic pulse pressure was positively correlated with the number of vessels involved (P = 0.0024). The results of the present study indicate that aortic pulse pressure is significantly and independently correlated with angiographically determined coronary artery stenosis.
Evaluating blood pressure response during exercise rather than during rest might better detect a subtle impairment in relaxation of the resistance vessel in hypercholesterolemia. We examined the relation between serum cholesterol and blood pressure response during exercise in patients with coronary artery disease. One hundred and forty-eight consecutive patients with coronary artery disease were monitored during symptom-limited incremental exercise testing with a cycle ergometer. Cuff blood pressure was measured every minute during exercise testing with an automatic indirect manometer. Although there were no significant differences in systolic or diastolic blood pressure at rest between the patients with hypercholesterolemia (total cholesterol ≥ 220 mg/dL, n = 39) and those without it (n = 109), the former reached a higher diastolic blood pressure at peak exercise (94.8 ± 16.0 versus 87.8 ± 12.9 mmHg, P = 0.007). The increase in diastolic blood pressure at peak exercise versus the resting value in the patients with hyper-cholesterolemia was 20.6 ± 11.3 mmHg, and this was significantly higher than the increase in patients without hypercholesterolemia (14.8 ± 11.8 mmHg, P = 0.009). However, there were no differences in the peak exercise systolic blood pressure and the magnitude of the increase in systolic blood pressure between the two groups. Among the patients with coronary artery disease in our study, we found that those with hypercholesterolemia had significantly higher diastolic blood pressure during exercise than those without hypercholesterolemia, strongly suggesting that patients with hyperlipidemia are at a higher risk of developing hypertensive complications.
Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.
Coronary artery anomalies are found in 0.6% to 1.5% of coronary angiograms. Angiographic recognition of these vessels is important because of their clinical significance and importance in patients undergoing coronary angioplasty or cardiac surgery. We reviewed the database of the Cardiac Catheterization Laboratory of Uludag Medical University in Bursa, Turkey. All patients who were subjected to coronary angiography from 1994 to 2001 were included. The study included 12,059 patients who underwent diagnostic coronary arteriography during the 8 year period. One hundred patients had primary congenital coronary anomalies. Ninty-five (95%) of the patients had anomalies of origin and distribution while five (5%) had coronary artery fistulae. The left main coronary artery (LMCA) was the most common anomalous vessel involved (forty-eight (48%) of the patients). An LMCA distribution anomaly was observed in these 48 patients. An anomalous right coronary artery (RCA) was the second most common anomaly, seen in twenty-two (22%) of the patients. An anomalous circumflex artery (Cx) was the third most common anomaly, seen in seventeen. Five patients had a coronary artery fistulae. The fistulae in our series were small without significant shunt circulation. Primary congenital coronary anomalies are isolated lesions and generally have no relation with other congenital heart diseases. They do not appear to be associated with an increased risk for development of coronary atherosclerosis. Angiographic recognition of these vessels is important because of their clinical significance and importance in patients undergoing coronary angioplasty or cardiac surgery.
We report a single center experience of surgical treatment of 30 cases of left-sided prosthetic valve thrombosis (PVT). In our series, a diagnosis of PVT was established based on clinical and echocardiographic examinations. Thrombosis was the major etiologic factor in 25 patients (83.3%), while 22 of 25 patients (88%) had a subtherapeutic anticoagulation level. The early hospital mortality rate was 7.1% in patients with New York Heart Association (NYHA) functional classes II - III, and 31.3% in NYHA functional class IV. The median interval from the surgical procedure to follow-up for these patients was 29.2 months. No recurrence or deaths were observed during 3 to 73 months following the surgical procedure.
The use of immunosuppressive therapy for inflammatory cardiomyopathy is controversial. The aim of this review is to summarize the current empirical evidence for immunosuppressive treatment in inflammatory cardiomyopathy. We conducted a meta-analysis of all randomized controlled trials (RCTs) that compared immunosuppressive therapy with either placebo or conventional treatment in patients with inflammatory cardiomyopathy. The pooled outcomes were all-cause death and heart transplantation for inflammatory cardiomyopathy, left ventricular ejection fraction (LVEF), and left ventricular end diastolic dimension (LVEDD). Five trials involving 316 patients were included. Overall, immunosuppressive therapy was not superior to placebo and conventional therapy in the pooled outcome of all-cause death and heart transplantation (odds ratio [OR] 1.03, 95% confidence intervals [CI] 0.58 to 1.80) in the long-term. The pooled data showed that there might be a short-term beneficial effect on LVEF improvement (5.06%, 95% CI -0.07% to 10.18%) in patients receiving immunosuppressive therapy, but no beneficial effect on LVEDD either in the short-term (-0.87 mm; 95% CI, -8.29 to 6.55 in adult patients) or long-term (-0.52 mm, 95% CI -3.64 to 2.60 in adult patients) was observed. There is no evidence to suggest that immunosuppressive therapy has an effect on improving the survival of patients with inflammatory cardiomyopathy. Current therapy in inflammatory cardiomyopathy seems to be limited to supportive measures or transplantation.
Left atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated. The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing. Forty-four patients with a left ventricular end-diastolic dimension (LVDd) ≥ 60 mm and an ejection fraction (EF) ≤ 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO2) (group 1: peak VO2 >14 mL/kg/min, group 2: peak VO2 ≤ 14 mL/kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF). LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO2. The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure.
A newly designed multiplaned mechanical aortic valve was created in which there would be an angle between the stents so the valve would have a greater orifice area. This study was performed to test this valve on bovine aorta to determine whether or not there would be a pressure gradient on both sides of the valve. The valve created is multiplaned with one stent thought to be seated on the aortic annulus for the coronary orifices to receive blood in diastole, whereas the other stent is thought to be seated on the ascending aorta obliquely to increase the orifice area of the valve. The ascending aorta could be enlarged if necessary. A multiplaned valve resembling the valve which has two planes was tested on a Dacron tube, one side of which was formed with a bovine aorta. Pressure readings before and after the bovine aorta was thinned were taken when a 17 L/min flow through the tube was maintained. A 65 mmHg mean pressure gradient and a zero pressure gradient were produced before and after thinning the bovine aorta. The multiplaned mechanical aortic valve produces no gradient if the aorta is elastic. This valve can solve the gradient problem in aortic valve surgery because the aorta is a living and elastic tissue.
No-reflow phenomenon is frequently observed during percutaneous coronary intervention in patients with acute coronary syndrome. It may jeopardize hemodynamic status or result in ischemic chest pain in these patients. Currently, there is no adequate solution for this problem. We report our experience with an acute coronary syndrome patient who developed no-reflow phenomenon associated with ST segment elevation and shock after percuteneous coronary balloon dilatation and stent deployment. Intracoronary administration of tirofiban immediately restored the coronary flow of the target vessel, and the disastrous condition reversed. Our experience suggests that intracoronary administration of tirofiban can be considered as an option in case of no-reflow phenomenon during percutaneous coronary intervention.
There is a syndrome consisting of acute infarction-like symptoms and ECG findings, and transient left ventricular apical ballooning without epicardial coronary artery obstruction. A 67-year-old female admitted to our hospital because of severe anterior chest pain was diagnosed as having this syndrome. Since stenotic, spastic, or occlusive sites were not found in epicardial coronary arteries by emergency cardiac catheterization, we speculated coronary microvasculature involvement in the pathophysiology of the event. Four weeks later in a drug-free condition, there was no significant epicardial coronary vasospasm by intracoronary acetylcholine administration (IC-ACh). The average peak flow velocity (APFV) of the left coronary artery (LCA) was measured using the Doppler flow wire method. Under maximal dilatation of the epicardial LCA by intracoronary nitroglycerin administration, IC-ACh was again performed taking into consideration that the change in APFV in response to IC-ACh reflects a coronary microvascular response to it. In the nonischemic control subjects, basal APFV increased to 296 ± 29% (n = 24) of the basal value after IC-ACh. In this patient, although IC-ACh did not cause vasospasm in epicardial LCA, APFV was decreased to 54% of its basal value. After administration of a Ca antagonist and KATP opener, she had no chest symptoms and was discharged from the hospital. In 2003, she forgot to take her medication for 3 days and then experienced a sudden recurrence of the same type of attack. She started her medication again and her symptoms disappeared. Three weeks later, she underwent an assessment of the coronary microvascular response to ACh with medicine. Her APFV after ACh increased to 177% of the basal value.
Congenital nonfamilial supravalvular aortic stenosis (SVAS) is relatively rare, its diffuse type being the least common. We present a 30-year-old woman with diffuse SVAS complicated with left ventricular apical aneurysm. We believe that subtle left ventricular myocardial ischemia or infarction and long-lasting severe pressure overload to the apical chamber caused LV apical aneurysm in our case. Acquired LV apical aneurysm secondary to supravalvular aortic stenosis, in the absence of atherosclerotic coronary artery disease and hypertrophic obstructive cardiomyopathy, has not been described before.
Left ventricular diverticulum is a rare congenital anomaly. In the adult population, the incidence was reported to be 0.26% in nonselected patients who underwent cardiac catheterization. Diverticula are usually localized near the apex and most often involve the inferior or anterior parietal walls of the left ventricle. In this report, two cases with congenital left ventricular diverticulum are presented, and the pathophysiologic, diagnostic, and therapeutic approaches of this cardiac malformation are discussed.
A male patient with tetralogy of Fallot accompanied by aortic regurgitation had maintained sufficient exercise capacity for a number of decades with the status of acyanotic tetralogy of Fallot. When he was 67 years old, he suffered a posterior wall acute myocardial infarction and direct percutaneous coronary angioplasty successfully revascularised the target lesion in the left circumflex artery. However, a few months after the onset of the myocardial infarction, his shortness of breath became clinically significant and was associated with increased right-to-left shunt and increased right ventricular end-diastolic pressure, as well as hypoxia. At 68 years old, therefore, total corrective repair of the tetralogy with replacement of the aortic and pulmonary valves was performed. The patient was asymptomatic after the successful operation. This report suggests that coronary artery disease can be one of the potential factors in inducing critical hemodynamic changes in aging patients with congenital heart disease, especially those who have a shunt between the right and left chambers. The unique clinical course is described with some discussion of the repair of tetralogy in adults.
Bleeding from suture holes in aortic valve replacement (AVR) may represent a difficult problem especially if the aortic wall is friable. We describe a case in which suture hole bleeding after AVR was present at the posterior aortic wall close to the pulmonary artery. Following several attempts to suture the leak using felt pledget armed prolene sutures, deep hypothermic circulatory arrest was induced and BioGlueTM in combination with Tabotamp TM was applied for successful sealing of the bleeding source.