Albert J. DeLuca

Efficacy of 3‐Hydroxy‐3‐Methylglutaryl Coenzyme A Reductase Inhibitors for Prevention of Stroke

OBJECTIVE: To determine if 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are effective in preventing fatal and nonfatal strokes in patients at increased risk of coronary artery disease.DESIGN: Meta-analysis of randomized controlled trials. Clinical trials were identified by a computerized search of medline (1983 to June 1996), by an assessment of the bibliographies of published studies, meta-analyses and reviews, and by contacting pharmaceutical companies that manufacture statins. Trials were included in the analysis if their patients were randomly allocated to a statin or placebo group, and reported data on stroke events. Thirteen of 28 clinical trials were selected for review. Data were extracted for details of study design, patient characteristics, interventions, duration of therapy, cholesterol measurements, and the number of fatal and nonfatal stroke events in each arm of therapy. Missing data on stroke events were obtained by contacting the investigators of the clinical trials.MAIN RESULTS: Among 19,921 randomized patients, the rate of total stroke in the placebo group was 2.38% (90% nonfatal and 10% fatal). In contrast, patients who received statins had a 1.67% stroke rate. Using an exact stratified analysis, the pooled odds ratio (OR) for total stroke was 0.70 (95% confidence interval [CI] 0.57, 0.86; p=.0005). The pooled OR for nonfatal stroke was 0.64 (95% CI 0.51, 0.79; p=.00001), and the pooled OR for fatal stroke was 1.25 (95% CI 0.71, 2.24; p=.4973). In separate analyses, reductions in total and nonfatal stroke risk were found to be significant only for trials of secondary coronary disease prevention. Regression analysis showed no statistical association between the magnitude of cholesterol reduction and the relative risk for any stroke outcome.CONCLUSIONS: The available evidence clearly shows that HMG-CoA reductase inhibitors reduce the morbidity associated with strokes in patients at increased risk of cardiac events. Data from 13 placebo-controlled trials suggest that on average one stroke is prevented for every 143 patients treated with statins over a 4-year period.

Comparison of sensitivity, specificity, positive predictive value, and negative predictive value of stress testing versus 64-multislice coronary computed tomography angiography in predicting obstructive coronary artery disease diagnosed by coronary angiography.

Sixty-four-multislice coronary computed tomographic angiography (CTA) and coronary angiography were performed in 145 patients (mean age 67 +/- 10 years), and stress testing was performed in 47 of these patients to determine the sensitivity, specificity, positive predictive value, and negative predictive value of coronary CTA and of stress testing in diagnosing obstructive coronary artery disease (CAD) in patients with suspected CAD. In 145 patients, coronary CTA had 98% sensitivity, 74% specificity, 90% positive predictive value, and 94% negative predictive value in diagnosing obstructive CAD. In 47 patients, stress testing had 69% sensitivity, 36% specificity, 78% positive predictive value, and 27% negative predictive value for diagnosing obstructive CAD, whereas coronary CTA had 100% sensitivity, 73% specificity, 92% positive predictive value, and 100% negative predictive value for diagnosing obstructive CAD. In conclusion, coronary CTA has better sensitivity, specificity, positive predictive value, and negative predictive value than stress testing in diagnosing obstructive CAD.

Anomalous origin of the left main coronary artery from the right sinus of Valsalva with an intramural course identified by transesophageal echocardiography in a 14 year old with acute myocardial infarction.

Coronary artery anomalies have an incidence of 0.6%1 to 1.3%2 in angiographic studies and 0.3%3 in an autopsy series. Anomalous origin of the left main coronary artery (LMCA) from the right sinus of Valsalva (RSOV) represents a small fraction (1.3%)2 of these anomalies, with an overall prevalence of 0.017%2 to 0.03%4 in angiographic studies. The high incidence of sudden cardiac death associated with this specific anomaly during or immediately after vigorous physical exercise makes identification and appropriate surgical intervention critical.2,5–10 We present a case report of a 14-year-old patient with an LMCA arising from the RSOV with an initial intramural course, presenting with acute myocardial infarction (AMI) as the first indication of the anomaly. Transthoracic echocardiogram suggested this anomaly, which was confirmed by cardiac catheterization and transesophageal echocardiogram.

Relation of Bone Mineral Density to Stress Test–Induced Myocardial Ischemia

Dual-energy x-ray absorptiometric scans of the spine and left hip were performed before stress testing for myocardial ischemia in 629 women and 136 men (mean age 63 years) with chest pain and no previous coronary artery disease. Of the 765 patients, 254 (33%) had osteoporosis, 260 (34%) had osteopenia, and 251 (33%) had normal bone mineral density (BMD). Stress test-induced myocardial ischemia was present in 95 of 254 patients (37%) with osteoporosis, in 81 of 260 patients (31%) with osteopenia, and in 62 of 251 patients (25%) with normal BMD (p = 0.002 comparing osteoporosis with normal BMD and p = 0.007 comparing osteoporosis or osteopenia with normal BMD). Stepwise logistic regression analysis showed that patients with osteoporosis or osteopenia had a 1.7 times higher chance of stress test-induced myocardial ischemia than those with normal BMD after controlling the confounding effects of systemic hypertension, diabetes mellitus, body mass index, and age. In conclusion, patients with chest pain undergoing stress testing have a higher prevalence of stress test-induced myocardial ischemia if they have osteoporosis or osteopenia than if they have normal BMD.

Incidence of Myocardial Infarction or Stroke or Death at 47‐Month Follow‐Up in Patients With Diabetes and a Predicted Exercise Capacity ≤85% vs >85% During an Exercise Treadmill Sestamibi Stress Test

A treadmill exercise sestamibi stress test (TESST) was performed in 609 consecutive diabetic persons with a mean age of 70 years and no history of coronary artery disease (CAD) who were referred for a TESST because of chest pain or dyspnea. Of 609 patients, 301 (49%) had a predicted exercise capacity <or=85% (group A) and 308 (51%) had a predicted exercise capacity >85% (group B). Group A patients had a higher prevalence of myocardial ischemia (43% vs 30%, P=.0005), 2- or 3-vessel obstructive CAD (38% vs 18%, P=.001), myocardial infarction (17% vs 9%, P=.004), death (10% vs 4%, P=.008), and myocardial infarction or stroke or death at 47-month follow-up (21% vs 12%, P=.001). Stepwise Cox regression analysis showed that the only significant independent predictor for the time to development of myocardial infarction or stroke or death was a predicted exercise capacity >85% (hazard ratio, 0.52; 95% confidence interval, 0.34-0.78; P=.002). Diabetic persons with a predicted exercise capacity >85% had a 48% lower chance of myocardial infarction, stroke, or death than those with a predicted exercise capacity <or=85%.

Systolic compression of left main coronary artery by left ventricular pseudoaneurysm complicated by critical stenosis of left main coronary artery

A 69-year-old man was admitted to the hospital with complaints of exertional substernal chest pain and dyspnea for 3 weeks. His medical history consisted of dyslipidemia, type 2 diabetes mellitus, and valvular heart disease. He had a mitral commissurotomy through a left thoracotomy for mitral stenosis at age 16 years followed by mitral valve replacement with a 25 mm Carpentier Edwards bovine pericardial prosthesis in February, 2007. He also had a aortic valve replacement with a 19 mm Carpentier Edwards bovine pericardial prosthesis at that time. On this admission, he had a maximum troponin I level of 0.12 (normal < 0.05 ng/ml), a creatine kinase-MB fraction of 3.4 (normal < 5.0 ng/ml), and a creatine phosphokinase of 288 (normal 35-232 U/l). Coronary angiography revealed near complete systolic obliteration of the left main coronary artery with normal caliber in diastole and discrete stenosis of the mid left anterior descending coronary artery resulting in 40% obstruction of the vessel (Figure 1A). Left ventriculography revealed systolic aneurysmal dilatation of a segment of the left ventricle (LV) compressing the left main coronary artery in systole and a LV ejection fraction of 50% (Figure 1B). Figure 1 Findings on the initial cardiac catheterization. A – Baseline coronary angiogram in left anterior oblique caudal view demonstrating systolic compression of the left main coronary artery (LM). B – Left anterior oblique cranial view of initial ... A thoracic computed tomography (CT) scan and a transesophageal echocardiogram (TEE) were obtained to provide anatomical delineation of the LV pseudoaneurysm The thoracic CT scan revealed an abnormal 3 cm × 2.4 cm contrast-filled structure to the left of the aorta, superior to the LV outflow tract, and inferior to the left main coronary artery likely representing a LV pseudoaneurysm. The TEE showed a normal LV ejection fraction, a small inferoposterior wall hypokinesis, and a LV pseudoaneurysm with a 1.3 cm opening originating below the mitral annulus anteriorly adjacent to the left atrial appendage extending superiorly to the left main coronary artery. The patient subsequently had a bovine patch repair of the LV pseudoaneurysm with resection of the left atrial appendage. A coronary angiogram obtained after surgery demonstrated a discrete fixed stenosis of the mid left main coronary artery resulting in 70% obstruction of the vessel (Figure 2). Intravascular ultrasound of the left main coronary artery stenosis revealed a cross sectional area of 2.9 mm2. Figure 2 Coronary angiogram in right anterior oblique caudal view of LM after resection of LV pseudoaneurysm showing evidence of critical LM stenosis The left main coronary artery was predilated with a 3.5 mm × 9 mm balloon inflated to 8 atm for 6 s. The stenosis was treated with a 4.0 mm × 12 mm everlimus drug-eluting stent that was deployed at 8 atm for 12 s with excellent results (Figures 3 and ​and4).4). Intravascular ultrasound imaging after percutaneous coronary intervention revealed a well apposed stent. Figure 3 Coronary angiogram displaying deployment of 4.0 mm × 12 mm PROMOS stent to the LM on right anterior oblique caudal view Figure 4 Right anterior oblique cranial view of LM after deployment of 4.0 mm × 12 mm PROMOS stent. after percutaneous coronary intervention (post PCI) A LV pseudoaneurysm is an incomplete rupture of the LV myocardium that is contained by organized LV thrombus, adherent scar tissue, and portions of the epicardum and parietal pericardium. In comparison to a true LV aneurysm, the LV pseudoaneurysm has a maximal neck to internal orifice width ratio of ≤ 0.5, a saccular or globular chamber, and a turbulent Doppler flow pattern through the neck [1]. The LV pseudoaneurysm can drain off significant portions of each LV stroke volume. A LV pseudoaneurysm can develop due to transmural myocardial infarction, previous ventriculotomy, replacement of the mitral valve, trauma, or infective endocarditis. It occurs in 0.02% to 2.0% of mitral valve replacement surgeries. Factors predisposing to LV psudoaneurysm include resection of the posterior leaflet of the mitral valve, excessive decalcification of the mitral annulus, placement of an oversized mitral valve prosthesis, and reoperation for mitral valve replacement [2]. The LV pseudoaneurysm following mitral valve replacement tends to be subannular in location [3]. Congestive heart failure, chest pain, and dyspnea are the most frequently reported symptoms associated with LV pseudoaneurysm. Approximately 70% of patients have systolic heart murmurs. A pansystolic murmur due to leaking of blood into the LV pseudoaneurysm may be heard on auscultation [4]. The majority of patients have electrocardiographic abnormalities which are usually nonspecific ST-segment changes. Lethal complications of LV pseudoaneurysm are LV failure, LV thrombus formation, embolization, rupture of the aneurysm and death [5]. To the best of our knowledge, there is only one published case of a patient with a history of open mitral commissurotomy and annuloplasty, aortic valve and mitral valve replacement presenting with chest pain and dyspnea with subsequent development of a LV pseudoaneurysm causing systolic compression of the left main coronary artery [6]. Unique to our case was critical left main coronary artery stenosis seen on coronary angiography after surgery which was successfully treated with percutaneous coronary intervention.

Comparison of two-dimensional echocardiographic tissue harmonic imaging and gated sestamibi single-photon emission computed tomographic left ventricular ejection fraction measurements

There was good correlation between left ventricular ejection fraction (EF) measurements employing 2-dimensional echocardiography with tissue harmonic imaging and single-photon emission computed tomography using quantitative gated scintigraphy, although in most patients, echocardiographic EF was lower. There was a high degree of agreement between these 2 techniques in assignment of EF to the categories of normal, mildly, moderately, or severely decreased. However, when EF categories did differ, echocardiography always resulted in assignment to a lower category.

Association of coronary artery calcium with severity of myocardial ischemia in left anterior descending, left circumflex, and right coronary artery territories.

An increasing coronary artery calcium score is associated with a higher likelihood of myocardial ischemia.

COMPARISON OF LEFT VENTRICULAR EJECTION FRACTION BY SINGLE PHOTON COMPUTED TOMOGRAPHIC MYOCARDIAL PERFUSION IMAGING VERSUS CORONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY

Introduction: Measurement of left ventricular (LV) ejection fraction by coronary computed tomography angiography (CTA) vs. single photon computed tomographic myocardial perfusion imaging (MPI) needs to be investigated. Material and methods: Myocardial perfusion imaging and CTA were performed in 292 patients because of chest pain or dyspnea. The patients included 178 men and 114 women, mean age 66 ±11 years. Results: The mean LV ejection fraction was 61 ±12% for the MPI tests and 65 ±11% for CTA (p <0.001). The LV ejection fraction was ≥ 50% in 250 of 292 patients (86%) with MPI testing and in 266 of 292 patients (91%) with CTA (p < 0.05). The LV ejection fraction was 36-49% in 31 of 292 patients (11%) with MPI testing and in 22 of 292 patients (8%) with CTA (p not significant). The LV ejection fraction was ≤ 35% in 11 of 292 patients (4%) with MPI testing and in 4 of 292 patients (1%) with CTA (p not significant). Pearson correlation coefficient was R = 0.67, p < 0.001. Conclusions: The resting LV ejection fraction is significantly higher in patients measured by CTA than in patients measured by MPI testing when both tests are performed in the same patients.