Papillary muscle rupture following acute myocardial infarction: Anatomic, echocardiographic, and surgical insights.

Papillary muscle (PM) rupture is a rare complication of acute myocardial infarction which carries an excessive mortality rate. Optimal outcomes require rapid diagnosis and prompt surgical referral, and in this regard, echocardiography plays a crucial role. Comprehensive echocardiographic examination of the patient with PM rupture consists of identification of the ruptured PM segment, visualization of flail mitral valve segment(s), evaluation of mitral regurgitation severity, and assessment of left ventricular systolic function. This article discusses anatomic and echocardiographic features as well as the surgical management of PM rupture.

Characteristics of plaque disruption by intravascular ultrasound in women presenting with myocardial infarction without obstructive coronary artery disease.

BACKGROUND: In a prospective study, we previously identified plaque disruption (PD: plaque rupture or ulceration) in 38% of women with myocardial infarction (MI) without angiographically obstructive coronary artery disease (CAD), using intravascular ultrasound (IVUS). Underlying plaque morphology has not been described in these patients and may provide insight into the mechanisms of MI without obstructive CAD. METHODS: Forty-two women with MI and <50% angiographic stenosis underwent IVUS (n = 114 vessels). Analyses were performed by a blinded core laboratory. Sixteen patients had PD (14 ruptures and 5 ulcerations in 18 vessels). Plaque area, % plaque burden, lumen area stenosis, eccentricity, and remodeling index were calculated for disrupted plaques and largest plaque by area in each vessel. RESULTS: Disrupted plaques had lower % plaque burden than the largest plaque in the same vessel (31.9% vs 49.8%, P = .005) and were rarely located at the site of largest plaque (1/19). Disrupted plaques were typically fibrous and were not more eccentric or remodeled than the largest plaque in the same vessel. CONCLUSIONS: Plaque disruption was often identifiable on IVUS in women with MI without obstructive CAD. Plaque disruption in this patient population occurred in fibrous or fibrofatty plaques and, contrary to expectations based on prior studies of plaque vulnerability, did not typically occur in eccentric, outwardly remodeled, or soft plaque in these patients. Plaque disruption rarely occurred at the site of the largest plaque in the vessel. These findings suggest that the pathophysiology of PD in women with MI without angiographically obstructive CAD may be different from MI with obstructive disease and requires further investigation.

In-stent thrombosis following DDAVP administration: case report and review of the literature.

A 67-year-old man with a drug-eluting stent in his proximal left anterior descending artery was admitted to the hospital after sustaining a traumatic injury to the skull. Due to persistent bleeding from a subgaleal hematoma, intravenous 1-desamino-8-D-arginine vasopressin (DDAVP) was administered. Five hours later, the patient complained of crushing chest pain. A 12-lead electrocardiogram demonstrated 2 mm ST-segment elevations in the precordial leads with reciprocal depressions in the inferior leads. Emergency cardiac catheterization demonstrated total occlusion of the proximal left anterior descending stent with TIMI 0 flow. Another drug-eluting stent was placed inside the original stent with restoration of TIMI 3 flow. During the catheterization, the patient became progressively hypoxic and hypotensive requiring intubation, dopamine drip, and placement of an intra-aortic balloon pump. The patient's hospitalization was complicated by prolonged shock requiring inotropes and vasopressors. This is the first reported case of an ST-elevation myocardial infarction due to in-stent thrombosis occurring after DDAVP administration. Though DDAVP is well tolerated and efficacious in treating several types of coagulopathies, this case illustrates its potential pro-thrombotic effects. Therefore, DDAVP should be used with caution in patients with known coronary artery disease and coronary stents.

Mechanisms of myocardial infarction in women without angiographically obstructive coronary artery disease.

BACKGROUND: There is no angiographically demonstrable obstructive coronary artery disease (CAD) in a significant minority of patients with myocardial infarction, particularly women. We sought to determine the mechanism(s) of myocardial infarction in this setting using multiple imaging techniques. METHODS AND RESULTS: Women with myocardial infarction were enrolled prospectively, before angiography, if possible. Women with ≥50% angiographic stenosis or use of vasospastic agents were excluded. Intravascular ultrasound was performed during angiography; cardiac magnetic resonance imaging was performed within 1 week. Fifty women (age, 57±13 years) had median peak troponin of 1.60 ng/mL; 11 had ST-segment elevation. Median diameter stenosis of the worst lesion was 20% by angiography; 15 patients (30%) had normal angiograms. Plaque disruption was observed in 16 of 42 patients (38%) undergoing intravascular ultrasound. There were abnormal myocardial cardiac magnetic resonance imaging findings in 26 of 44 patients (59%) undergoing cardiac magnetic resonance imaging, late gadolinium enhancement (LGE) in 17 patients, and T2 signal hyperintensity indicating edema in 9 additional patients. The most common LGE pattern was ischemic (transmural/subendocardial). Nonischemic LGE patterns (midmyocardial/subepicardial) were also observed. Although LGE was infrequent with plaque disruption, T2 signal hyperintensity was common with plaque disruption. CONCLUSIONS: Plaque rupture and ulceration are common in women with myocardial infarction without angiographically demonstrable obstructive coronary artery disease. In addition, LGE is common in this cohort of women, with an ischemic pattern of injury most evident. Vasospasm and embolism are possible mechanisms of ischemic LGE without plaque disruption. Intravascular ultrasound and cardiac magnetic resonance imaging provide complementary mechanistic insights into female myocardial infarction patients without obstructive coronary artery disease and may be useful in identifying potential causes and therapies. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00798122.

Sex and race are associated with the absence of epicardial coronary artery obstructive disease at angiography in patients with acute coronary syndromes.

BACKGROUND: A substantial minority of patients with acute coronary syndromes (ACS) do not have a diameter stenosis of any major epicardial coronary artery on angiography ("no obstruction at angiography") of > or = 50%. We examined the frequency of this finding and its relationship to race and sex. HYPOTHESIS: Among patients with myocardial infarction, younger age, female sex and non-white race are associated with the absence of obstructive coronary artery disease at angiography. METHODS: We reviewed the results of all angiograms performed from May 19, 2006 to September 29, 2006 at 1 private (n = 793) and 1 public (n = 578) urban academic medical center. Charts were reviewed for indication and results of angiography, and for demographics. RESULTS: The cohort included 518 patients with ACS. There was no obstruction at angiography in 106 patients (21%), including 48 (18%) of 258 patients with myocardial infarction. Women were more likely to have no obstruction at angiography than men, both in the overall cohort (55/170 women [32%] vs 51/348 men [15%], P < 0.001) and in the subset with MI (29/90 women [32%] vs 19/168 men [11%], P < 0.001). Black patients were more likely to have no obstruction at angiography relative to any other subgroup (24/66 [36%] vs 41/229 [18%] Whites, 31/150 [21%] Hispanics, and 5/58 [9%] Asians, P = 0.001). Among women, Black patients more frequently had no obstruction at angiography compared with other ethnic groups (16/27 [59%] vs 17/59 [29%] Whites, 17/60 [28%] Hispanics, and 3/19 [6%] Asians, P = 0.001). CONCLUSIONS: A high proportion of a multiethnic sample of patients with ACS were found to have no stenosis > or = 50% in diameter at coronary angiography. This was particularly common among women and Black patients.

Long-term outcomes in non-diabetic patients with metabolic syndrome undergoing revascularization for multi-vessel coronary artery disease.

AIM: The influence of metabolic syndrome (MS) on long-term mortality and morbidity in multi-vessel coronary artery disease (MV-CAD) is unclear. We studied the impact of MS on long-term outcomes in non-diabetic patients (NDM) with MV-CAD undergoing coronary revascularization in the Bypass Angioplasty Revascularization Investigation (BARI) trial and registry. METHODS: BARI trial and registry patients were separated into those with diabetes (DM) and those without. NDM fulfilling the NCEP definition of MS were identified. Ten year follow-up data were obtained on mortality, MI and development of diabetes. The data were analyzed using Cox proportional hazard modeling. RESULTS: In the BARI trial and registry 2962 NDM were identified. Of those, 510 patients had 3 or more components of the BARI-modified NCEP definition for MS, while 445 patients had 2 components of the definition and were classified as the "mixed group". Compared to patients without MS, both MS group (RR=3.2, p<0.0001) and the mixed group (RR=1.9, p=0.02) had a higher incidence of DM over the 10-year follow-up. Type 2 DM was found to be highly associated with 10-year mortality (RR=1.65, p<0.0001). However, there was no statistically significant difference in the rate of death or MI at 5 and 10 years between NDM with or without MS. In multivariate analysis, the presence of MS was not associated with 10-year mortality in the BARI population (RR=0.93, p=0.62). CONCLUSION: In this BARI follow-up study, we have affirmed the role of MS in predicting the development of diabetes in NDM at baseline. The 10-year risk of mortality and MI was not greater in NDM with MS who had MV-CAD and underwent revascularization, compared to patients without MS. Further studies to evaluate MS patients with MV-CAD undergoing coronary revascularization are warranted.

Access site hematoma requiring blood transfusion predicts mortality in patients undergoing percutaneous coronary intervention: data from the National Heart, Lung, and Blood Institute Dynamic Registry.

OBJECTIVE: To determine both the etiology of and outcomes associated with access site hematoma requiring transfusion (HRT) in patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: Access site hematoma in the setting of PCI is the most frequent periprocedural complication (2-12%). Antiplatelet and antithrombin therapy is designed to lower the incidence of adverse ischemic events while maintaining an acceptable rate of hemorrhagic complications. METHODS: This was a prospective, multi-center, cohort study of consecutive patients undergoing PCI during 3 NHLBI Dynamic Registry recruitment waves (1997-2002). The primary endpoints included the incidence of HRT, in-hospital death, and death at 1-year. RESULTS: The incidence of HRT was 1.8% and femoral access was common. Older age, lower BMI, female sex, concomitant renal, cerebrovascular, peripheral vascular, and pulmonary disease were significantly associated with HRT. Glycoprotein IIb/IIIa inhibitors, thrombolytic therapy, and postprocedure heparin were more commonly used in HRT patients, but there was no difference in thienopiridiene use. Attempted lesions in patients developing HRT were more often calcified, thrombotic, located in an ostial location, or class B2 or C. In-hospital mortality and 1-year death rate was 9 and 4.5 times higher in HRT patients respectively. Following adjustment, HRT remained independently associated with in-hospital mortality (OR 3.59, 95% CI 1.66-7.77) and 1-year death (hazard ratio [HR] 1.65, 95% CI 1.01-2.70, P = 0.048). Independent predictors of HRT included age, female sex, IIb/IIIa inhibitors, thrombolytic agents, and concomitant conditions. CONCLUSIONS: Access site complications, especially HRT, remain a very important predictor of adverse procedural success and patient outcome.

Ezetimibe: rationale and role in the management of hypercholesterolemia.

Elevated low-density lipoprotein (LDL) cholesterol plays an important role in the development of atherosclerosis. In part, plasma LDL levels are dependent on cholesterol absorption in the intestine and the rate of intrinsic cholesterol synthesis. Therapy with 3-hydroxy-3-methylglutaryl coenzyme A-reductase inhibitors has often proven to be successful in reducing plasma LDL levels. However, a significant number of patients do not reach their target LDL levels despite statin therapy. As is reviewed, drugs that inhibit cholesterol absorption are a useful adjunct to lipid-lowering therapy by statins. This review discusses the mechanisms involved in intestinal absorption of cholesterol and its transport as potential targets of newer agents that affect cholesterol absorption. The use of bile acid sequestrants and esters of plant stanols, as well as other intestinally active agents for reducing plasma LDL levels, has been limited by side effects and difficulties in patient compliance. In contrast, the new selective cholesterol transporter inhibitor ezetimibe has been demonstrated to reduce plasma LDL alone or in combination with statins without significant adverse effects. In spite of the robust lipid-lowering data with ezetimibe, questions about clinical outcomes, safety, and efficacy in various combinations remain.

Saphenous vein graft aneurysm masquerading as a right atrial mass.

We report a case of a large saphenous vein graft (SVG) aneurysm masquerading as a right atrial mass on transesophageal echocardiogram. Cardiac magnetic resonance angiography reliably made a diagnosis of SVG aneurysm extrinsically compressing right atrium. This case illustrates the importance of using combined imaging modalities for the diagnosis and management of cardiac masses.