Craig E. Monsen

Relation of Bone Mineral Density to Frequency of Coronary Heart Disease

Coronary angiography was performed because of chest pain in 198 patients (146 women, 52 men; mean age 66 years) who had dual-energy x-ray absorptiometry scans of the spine and left hip because of suspected osteoporosis or osteopenia. Of the 198 patients, 53 (27%) had osteoporosis, 79 (40%) had osteopenia, and 66 (33%) had normal bone mineral density (BMD). Obstructive coronary artery disease with >50% narrowing of > or =1 major coronary artery was present in 40 of 53 patients (76%) with osteoporosis, in 54 of 79 patients (68%) with osteopenia, and in 31 of 66 patients (47%) with normal BMD (p <0.005 comparing osteoporosis with normal BMD, p <0.01 comparing osteopenia with normal BMD). In conclusion, in patients who undergo coronary angiography because of chest pain, patients with osteoporosis or osteopenia have a higher prevalence of obstructive coronary artery disease than those with normal BMD.

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.

Intracoronary brachytherapy for treatment of in-stent restenosis.

Randomized, double-blind, placebo-controlled trials have demonstrated that intracoronary brachytherapy is more efficacious than placebo in reducing death, myocardial infarction, and target vessel revascularization at long-term follow up of patients with in-stent restenosis. Intracoronary brachytherapy is efficacious in treating totally occluded in-stent restenotic lesions, in treating de novo and in-stent restenotic lesions in saphenous vein grafts, in treating diffuse in-stent restenosis, in treating native coronary ostial in-stent restenotic lesions, in treating patients with diabetes with in-stent restenosis, in treating patients at high-risk for recurrence of restenosis, in treating elderly patients, and in treating patients who failed intracoronary radiation. Beta and gamma intracoronary brachytherapy are equally effective in treating in-stent restenosis. Long-term aspirin and clopidogrel should be administered for at least 1 year to reduce late vessel thrombosis. Inadequate radiation may cause edge stenosis.

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%.

Major adverse cardiac events in patients with moderate to severe renal insufficiency treated with first-generation drug-eluting stents.

No data are available comparing the long-term outcome of sirolimus-eluting stents (SESs) versus paclitaxel-eluting stents (PESs) in patients with moderate to severe renal insufficiency. The incidence of major adverse cardiac events (MACE), including death, myocardial infarction, and target vessel revascularization, during long-term follow-up were studied in patients with a glomerular filtration rate of <60 ml/min/1.73 m(2), as measured by the Modification of Diet in Renal Disease (MDRD) study equation, who also underwent percutaneous coronary intervention with drug-eluting stents. Of 428 patients studied, PESs were placed in 287 patients and SESs in 141 patients. Stepwise Cox regression analyses were performed to identify significant independent risk factors for MACE. At 47 + or - 19 months of follow-up, MACE had occurred in 49 (17%) of 287 patients in the PES group (mean age 71 + or - 11 years, 55% men) and in 31 (22%) of 141 patients in the SES group (mean age 71 + or - 12 years, 53% men). No significant difference was found in the MACE rate between the PES and SES groups. This persisted even after controlling for stent length, lesion complexity, and other co-morbidities. Also, all-cause mortality was not significantly different between the PES and SES groups (7.1% vs 8.5%, respectively). In conclusion, during long-term follow-up of patients with moderate to severe renal insufficiency, the rates of MACE and all-cause mortality were similar in the PES and SES groups.

Comparison of prevalence of >70% diameter narrowing of one or more major coronary arteries in patients with versus without mitral annular calcium and clinically suspected coronary artery disease.

The prevalence of >70% narrowing of 1, 2, or 3 major coronary arteries and of 3 major coronary arteries was investigated in 2,465 patients (1,437 men, 1,028 women; mean age 69 +/- 13 years) with severe, moderate, mild, or no mitral annular calcium (MAC) diagnosed by 2-dimensional echocardiography who underwent coronary angiography for suspected coronary artery disease. Greater than 70% narrowing of 1, 2, or 3 major coronary arteries was present in 259 of 315 patients (82%) with severe MAC (group 1), in 835 of 1,052 patients (79%) with moderate or mild MAC (group 2), and in 756 of 1,098 patients (69%) with no MAC (group 3) (p <0.001 comparing group 1 with group 3 and group 2 with group 3). Greater than 70% narrowing of 3 major coronary arteries was present in 149 of 315 patients (47%) in group 1, in 366 of 1,052 patients (35%) in group 2, and in 325 of 1,098 patients (30%) in group 3 (p <0.001 comparing group 1 with group 3 and group 1 with group 2; p <0.01 comparing group 2 with group 3). In conclusion, MAC is associated with obstructive >or=1-vessel coronary artery disease and with obstructive 3-vessel coronary artery disease.

Incidence of in-hospital mortality or nonfatal myocardial infarction or nonfatal stroke in 216 diabetics and 552 nondiabetics undergoing percutaneous coronary intervention with stenting.

We investigated the incidence of in-hospital mortality or nonfatal myocardial infarction or nonfatal stroke in 216 patients with diabetes mellitus and in 552 patients without diabetes mellitus (68% men and 32% women, mean age 66 ± 14 y) who underwent percutaneous coronary intervention with stenting. Symptomatic chest pain was present in 95% of diabetics and in 95% of nondiabetics. Unstable symptoms were present in 67% of diabetics and in 68% of nondiabetics. Aspirin was used in 99% of diabetics and nondiabetics. Clopidogrel was used in 98% of diabetics and nondiabetics. Beta blockers were used in 85% of diabetics and nondiabetics. Lipid-lowering drugs were used in 96% of diabetics and in 95% of nondiabetics. In-hospital mortality occurred in 2 of 216 diabetics (0.9%) and in 2 of 552 nondiabetics (0.4%), P not significant. In-hospital mortality or nonfatal myocardial infarction or nonfatal stroke occurred in 3 of 216 diabetics (1.4%) and in 6 of 552 nondiabetics (1.1%), P not significant.

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.

Risk factors for major bleeding and for minor bleeding after percutaneous coronary intervention in 634 consecutive patients with acute coronary syndromes.

Of 634 consecutive patients who had percutaneous coronary intervention (PCI) for acute coronary syndromes, 34 (5%) had major bleeding after PCI, 253 (40%) had minor bleeding after PCI, and 347 (55%) had no bleeding after PCI. Significant independent risk factors for major bleeding after PCI were increased troponin I level (P = 0.004; odds ratio [OR] = 4.7), prior coronary artery disease (P = 0.029; OR = 3.7), platelet glycoprotein IIb/IIIa inhibitors (P = 0.002; OR = 9.8), glomerular filtration rate (GFR) <30 versus ≥60 mL/min/1.73 m2 (P < 0.0001; OR = 39.7), GFR 30-59 versus ≥60 mL/min/1.73 m2 (P = 0.0001; OR = 9.4), and clopidogrel loading dose >300 mg (P = 0.0001; OR = 8.9). Significant independent risk factors for minor bleeding after PCI were increased troponin I level (P = 0.0004; OR = 2.1), platelet glycoprotein IIb/IIIa inhibitors (P = 0.039; OR = 2.4), GFR 30-59 versus ≥60 mL/min/1.73 m2 (P < 0.0001; OR = 2.5), thrombolytics (P = 0.01; OR = 2.7), clopidogrel loading dose >300 mg (P < 0.0001; OR = 4.2), and systolic blood pressure during PCI (P < 0.0001; OR = 1.03 per mm Hg). In-hospital deaths included 5 of 34 patients (15%) with major bleeding, none of 253 patients (0%) with minor bleeding, and none of 347 patients (0%) with no bleeding (P < 0.0001). Hospital duration was 11.0 days in patients with major bleeding, 3.4 days in patients with minor bleeding, and 1.8 days in patients with no bleeding (P < 0.0001).