Importance of papillary muscle infarction detected by cardiac magnetic resonance imaging in predicting cardiovascular events.

BACKGROUND: Recent studies suggest that papillary muscle infarction (PMI) following recent myocardial infarction (MI) correlates with adverse cardiovascular outcomes. The purpose of this study is to determine the prevalence and prognostic significance of PMI by cardiac magnetic resonance (CMR) in a large cohort of patients. METHODS: Retrospective study of patients who underwent CMR between January 2007 and December 2009 were evaluated for the presence of PMI in one or both of the left ventricle papillary muscles. The primary outcome was a time to a combined endpoint of all-cause mortality and worsening heart failure. Secondary outcomes were time to individual components of the combined outcome. RESULTS: 419 patients were included in our analysis, 232 patients (55%) had ischemic cardiomyopathy. Patients were followed at six-month intervals for a median follow-up time of 3.7 (interquartile range (IQR): 1.6; 6.3) years after initial imaging. During this period 196 patients (46.8%) had a primary outcome and 92 patients (22%) died. PM infarct was identified in 204 (48.7%) patients with twice as many posteromedial (PRM) (27%) than anterolateral (ARL) lesions (11%) and a similar number with infarct in both (11%). There was no association between studied outcomes and the presence of PMI in either PRM or ARL PM. The presence of infarct in both PM was a predictor of both the primary outcome (HR 1.69, CI[1.01-2.86], p<0.049.) and mortality (HR 1.69, CI[1.01-4.2], p<0.046). CONCLUSION: The presence of infarct in either papillary muscle was not associated with outcomes. However, infarct involving both papillary muscles was associated with worse outcomes.

The vasorelaxant hormone relaxin induces changes in liver sinusoid microcirculation: a morphologic study in the rat.

This study shows that specialized contractile endothelial cells exist in rat liver sinusoids which may be involved in the local control of hemodynamics and which are sensitive to vasoactive agents, including the vasorelaxant hormone relaxin. Male rats were treated with 10 microg relaxin for 4 days; phosphate-buffered saline (PBS)-treated rats were the controls. For comparison, rats treated with relaxin together with the NO-synthase inhibitor N(omega)-nitro-l -arginine methyl ester (L-NAME), and rats treated with the vasodilator taurodeoxycholic acid or the vasoconstrictor ethanol were investigated. Liver fragments were studied morphologically and morphometrically. In the control rats, peculiar contractile cells were present in the endothelial lining. These cells had abundant myofilaments and formed cytoplasmic blebs projecting into and often occluding the lumen. In the ethanol-treated rats, sinusoids were constricted and filled with cytoplasmic blebs. In the relaxin-treated rats, sinusoids were markedly dilated and the cytoplasmic blebs nearly disappeared. Similar findings were observed in the taurodeoxycholic acid-treated rats. The effects of relaxin were blunted by L-NAME, suggesting that the relaxin action involves an NO-mediated mechanism.

QT prolongation associated with azithromycin/amiodarone combination.

Administration of oral azithromycin, in addition to previously well-tolerated long-term amiodarone therapy, was associated with a marked prolongation of QT interval and increased QT dispersion, both substrates for life-threatening ventricular tachyarrhythmia and torsades de pointes. This is a report of QT prolongation and increased QT dispersion associated with the use of azithromycin. The report assumes an added significance, in view of widespread empirical use of this antibiotic for the treatment of lower respiratory infections and belief of its safety in patients with cardiac diseases. Based on the authors' experience, they would like to emphasize that the combination of azithromycin with other drugs known to prolong QT or causing torsades de pointes be used with caution until the question of the proarrhythmic effect of azithromycin is resolved by further studies.

Effect of acute myocardial infarction on cholesterol ratios.

OBJECTIVE: In patients with acute myocardial infarctions (MIs), cholesterol levels are no longer valid after 24 h from presentation because acute MI causes a rapid decline in serum levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. The objective of this study was to evaluate the effect of acute MI on the total cholesterol/HDL cholesterol ratio and the LDL cholesterol/HDL cholesterol ratio. METHODS: The study consisted of 45 patients who were admitted to the hospital with acute MIs. Serum levels of total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides were determined on day 1 post-MI and day 4 post-MI. The total cholesterol/HDL cholesterol ratio and the LDL cholesterol/HDL cholesterol ratio were calculated. Serum lipid levels and cholesterol ratios were compared between day 1 post-MI and day 4 post-MI. RESULTS: From day 1 post-MI to day 4 post-MI, the mean (+/- SD) serum levels of total cholesterol (188.4 +/- 52.5 vs. 170.5 +/- 57.2 mg/dL, respectively; p = 0.01), LDL cholesterol (120.3 +/- 48.9 vs. 105.9 +/- 43.0 mg/dL, respectively; p = 0.009), and HDL cholesterol (45.0 +/- 18.5 vs 39.3 +/- 16.1 mg/dL, respectively; p < 0.001) decreased, but the mean serum level of triglycerides (119.2 +/- 81.2 vs 149.3 +/- 68.3 mg/dL, respectively; p = 0.006) increased. The cholesterol ratios, however, remained unchanged between day 1 post-MI and day 4 post-MI. The total cholesterol/HDL cholesterol ratio was 4.59 +/- 1.84 on day 1 post-MI and 4.67 +/- 1.77 on day 4 post-MI (change not significant). The LDL cholesterol/HDL cholesterol ratio was 2.96 +/- 1.58 on day 1 post-MI and 2.99 +/- 1.44 on day 4 post-MI (change not significant). CONCLUSION: Acute MI does not affect the cholesterol ratios. Therefore, when the absolute levels of serum cholesterol are no longer valid (beyond 24 h after an MI), the cholesterol ratios still could be useful for cholesterol risk assessment in patients with acute MIs.

Prognostic value of serum cardiac troponin I in ambulatory patients with chronic renal failure undergoing long-term hemodialysis: a two-year outcome analysis.

OBJECTIVES: We sought to evaluate the prognostic value of cardiac troponin I (cTnI) in asymptomatic, ambulatory patients with chronic renal failure treated with long-term hemodialysis. BACKGROUND: Smaller, short-term follow-up studies on this subject have given conflicting results. METHODS: A total of 126 ambulatory patients with chronic renal failure treated with long-term hemodialysis were followed for two years for all-cause mortality, cardiac mortality, all-cause hospital admissions and cardiac hospital admissions. Serum cTnI was measured before dialysis at the time of study entry. RESULTS: One hundred two patients had normal serum levels of cTnI (< or =0.03 ng/ml) and 24 patients had elevated levels (0.015 +/- 0.007 vs. 0.053 +/- 0.029 ng/ml, p < 0.0001). No significant difference in all-cause mortality (20 vs. 4 deaths), cardiac mortality (4 vs. 1 death), all-cause hospital admissions (1.74 +/- 1.72 vs. 1.25 +/- 1.19 admissions/patient) or cardiac admissions (0.52 +/- 0.89 vs. 0.33 +/- 0.76 admissions/patient) was present between the patients with normal cTnI levels and those with elevated cTnI levels. Serum cTnI was not significantly different between patients who died versus those who survived (0.022 +/- 0.019 vs. 0.022 +/- 0.021 ng/ml). Serum cTnI was not an independent predictor of all-cause mortality, cardiac mortality, all-cause admissions or cardiac admissions. Age (older) and serum albumin (lower) were independent predictors of all-cause mortality, whereas a history of myocardial infarction was an independent predictor of cardiac mortality. Serum sodium (lower) was an independent predictor of all-cause hospital admissions, whereas hypertension and previous myocardial infarction were independent predictors of cardiac admissions. The best predictors of the time to death were age (older) and serum sodium level (lower), irrespective of the serum cTnI levels. CONCLUSIONS: Cardiac troponin I has a limited role in predicting mortality and hospital admissions in asymptomatic patients with chronic renal failure treated with long-term hemodialysis.

Anomalous circumflex coronary artery: benign or predisposed to selective atherosclerosis.

Anomalous origin of the circumflex coronary artery from the right sinus of Valsalva is the most common coronary anomaly and is usually considered benign. Although several researchers in the past believed that aberrancy predisposes this vessel to accelerated atherosclerosis, this could not get wide acceptance owing to lack of convincing data. To examine the suggestion that atherosclerosis affects the anomalous circumflex artery more severely, the authors reviewed the clinical and angiographic features of patients with this anomaly identified from 2,684 coronary angiography procedures performed between January 1998 and March 2000 at their institution. The degree of atherosclerotic narrowing in the anomalous artery was compared with that in other coronary arteries in the same patient as well as in the nonanomalous circumflex arteries in controls. For comparison 3 control subjects were selected for each patient with anomalous circumflex artery, matched by age, sex, and clinical presentations. The results showed earlier and greater degree of atherosclerotic narrowing of the anomalous artery as compared to the other coronary arteries in the same patients as well as to nonanomalous circumflex arteries of age- and gender-matched control subjects with similar clinical characteristics. However, this predilection for atherosclerosis was evident only in anomalous vessels arising from the right side and pursuing a retroaortic course. The anomalous artery was responsible for myocardial infarction in 3 patients, all of whom were 60 years or older. Two of the patients with this anomaly and myocardial infarction underwent successful angioplasty with stent placement for symptomatic relief.

Age-related differences in the use of cardiac medications in patients with coronary artery disease.

BACKGROUND: Benefits of aspirin and beta-blocker use in patients with coronary artery disease and angiotensin-converting enzyme (ACE) inhibitors in those with left ventricular systolic dysfunction are well documented in all age groups. OBJECTIVE: To investigate whether aspirin, beta-blockers, and ACE inhibitors are equally used in geriatric (> or =65 years) versus younger (<65 years) patients with coronary artery disease. SETTING: University-affiliated major academic hospital. METHODS: Records of 402 patients with coronary artery disease were analyzed for use of aspirin, beta-blockers, and ACE inhibitors. One hundred thirty patients with contraindications to use of these agents were excluded. RESULTS: Of 272 study patients, 85% were using aspirin and 71% beta-blockers. Among the patients with left ventricular systolic dysfunction, 79% were using ACE inhibitors. One hundred forty-seven patients were of geriatric age, whereas 125 were of younger age. No significant difference in the use of aspirin (82% versus 89%, P = 0.10), beta-blockers (71% versus 70%, P = 0.85), or ACE inhibitors (86% versus 69%, P = 0.13) was found between geriatric and younger patients. This lack of difference in use of cardiac medications between geriatric and younger patients persisted on gender-based subgroup analysis. On decade-of-age-based analysis, aspirin use was not equally distributed among all the decades of age (P < 0.005), but beta-blocker use was. CONCLUSION: Results of this study demonstrate equal use of aspirin, beta-blockers, and ACE inhibitors in geriatric versus younger patients with coronary artery disease. Aspirin use was not equally distributed among all the decades of age.

Atrial fibrillation associated with systemic lupus erythematosus and use of methylprednisolone.

Systemic lupus erythematosus is known to have cardiac manifestations consisting of pericarditis, myocarditis, endocarditis, and coronary vasculitis. Pericarditis is the most common cardiac manifestation of systemic lupus erythematosus. Myocarditis may be suspected in patients presenting with unexplained tachycardia, conduction disturbances, unexplained systolic dysfunction with or without heart failure, or arrhythmias. The development of arrhythmias in systemic lupus erythematosus could be secondary to pericarditis, myocarditis, or ischemia caused by coronary vasculitis. The development of atrial fibrillation in systemic lupus erythematosus is not commonly reported. There have been few reports on the patients developing atrial fibrillation after being started on methylprednisolone therapy. Described here is a case of the development of atrial fibrillation in a newly diagnosed 37-year-old patient with systemic lupus erythematosus who was started on intravenous methylprednisolone therapy.

Relaxin causes changes of the liver. In vivo studies in rats.

During pregnancy, the liver undergoes metabolic adjustments directed to fulfil the needs of the mother and the growing fetus. This study was designed to verify whether relaxin, a hormone related to pregnancy, may induce histochemical and ultrastructural modifications of hepatocytes which can be related to metabolic changes. Estrogen-primed female rats were treated with relaxin (10 microg in repository vehicle) for 18 h. Additional male rats were treated with relaxin (10 microg/day in PBS) for 4 days. Appropriate vehicle-treated rats were used as controls. After fasting, the rats were killed and liver fragments were processed for light and electron microscopy and for computer-assisted morphometry of PAS-positive glycogen deposits and acid phosphatase-reactive organelles. In both sexes, the relaxin-treated rats underwent a significant decrease in the amount of glycogen in the hepatocytes as compared with the controls. These changes were accompanied by an increase in smooth endoplasmic reticulum, endocytosis vesicles and lysosomes. These findings show that relaxin promotes glycogen depletion and induces morphological changes of hepatocytes which are consistent with functional activation. It is suggested that relaxin might play an important role in hepatic metabolic adjustments occurring during pregnancy.

Scleroderma pericardial disease presented with a large pericardial effusion--a case report.

Scleroderma pericardial disease is usually silent and benign. The incidence of pericardial involvement in scleroderma is about 50% according to autopsy results, but symptomatic pericarditis manifests in about 16% of patients with diffuse scleroderma and in about 30% of patients with limited scleroderma. The clinically evident pericardial effusion is rare in scleroderma, although it can be detected in about 41% of patients with echocardiography. In majority of the patients, the pericardial effusion is small and not associated with symptoms. The pericardial effusion manifests usually after the manifestation of the other clinical and serologic features of scleroderma. A case of scleroderma is reported that presented with a large pericardial effusion, which antedated the other clinical and serologic features of scleroderma. The pericardial involvement in scleroderma is reviewed.

Acute ventricular rate control in atrial fibrillation: IV combination of diltiazem and digoxin vs. IV diltiazem alone.

OBJECTIVE: To analyze the efficacy of an IV combination of diltiazem and digoxin vs IV diltiazem alone for acute ventricular rate control in patients with atrial fibrillation. DESIGN: Prospective, randomized, open-label study. PATIENTS AND METHODS: Fifty-two patients with atrial fibrillation and uncontrolled ventricular rates were randomized to receive either an IV combination of diltiazem and digoxin or IV diltiazem alone and were observed for 12 h. The successful rate control was defined as a ventricular rate < 100 beats per minute (bpm) persisting for 1 h or conversion to sinus rhythm. The loss of rate control was defined as an increase in the ventricular rate to > 100 bpm persistently for > 30 min or rebound to atrial fibrillation. RESULTS: In both treatment arms (n = 26 each), all patients achieved successful and comparable ventricular rate control at 12 h. The mean (+/- SD) time taken to achieve successful rate control was shorter in the combination arm (15 +/- 16 vs. 22 +/- 22 min). Six patients in the combination arm and 11 in the diltiazem-alone arm experienced episodes of loss of rate control. This loss in the combination arm was less than that in the diltiazem-alone arm (14 vs 39 episodes; p = 0.05). The loss of rate control per patient in the combination arm was also less than that in the diltiazem-alone arm (2.0 +/- 1.0 vs. 3.5 +/- 1.9 episodes per patient; p = 0.04). CONCLUSIONS: This study demonstrates that in patients with atrial fibrillation who have a rapid ventricular response, the IV combination of diltiazem and digoxin results in a more efficacious ventricular rate control with fewer fluctuations than that achieved by therapy with IV diltiazem alone.

Worsening of left ventricular diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension.

BACKGROUND: Exercise tolerance is reduced in hypertension. Hypertension affects left ventricular (LV) diastolic filling by causing abnormal relaxation and decreasing compliance. HYPOTHESIS: This study was designed to determine whether worsening of LV diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension. METHODS: Left ventricular diastolic filling parameters were examined at mitral valve by Doppler echocardiography at rest and at peak exercise in hypertensive patients and were compared with those of age- and gender-matched normotensive individuals. Treadmill exercise stress test was performed according to the Bruce protocol and the exercise time was recorded. RESULTS: Exercise time was significantly shorter in the hypertensive group than that in the normotensive group (320 +/- 29 vs. 446 +/- 38 s, p 0.03). The hypertensive group demonstrated abnormal relaxation pattern of diastolic mitral inflow at rest, which became pseudonormal at peak exercise (E/A velocity ratio, rest 0.86 +/- 0.06 vs. exercise 1.19 +/- 0.09, p < 0.001). The diastolic mitral inflow pattern remained normal at peak exercise in the normotensive group. The deceleration time and the pressure half time of early mitral inflow at peak exercise were significantly shorter in the hypertensive group than those in the normotensive group (deceleration time, 182 +/- 20 vs. 238 +/- 22 ms, p 0.02: pressure half time, 54 +/- 5 vs. 70 +/- 12 ms, p 0.01). CONCLUSIONS: This study demonstrates that reduced exercise tolerance in hypertension is associated with worsening of diastolic dysfunction during exercise consistent with an increase in left atrial pressure.

Nonatherosclerotic aneurysm of the left circumflex coronary artery presenting with accelerated angina pectoris: response to medical management--a case report.

Coronary artery aneurysm is defined as coronary dilatation with a diameter of more than 1.5 times the adjacent normal coronary artery. Most of the coronary aneurysms remain asymptomatic. More than 90% of coronary aneurysms are of atherosclerotic origin. Nonatherosclerotic coronary aneurysms are rare, and the majority of them are diffuse. Among the three major coronary arteries, the left circumflex artery is the least commonly involved. The management strategies for nonatherosclerotic coronary aneurysms are not clear, and each case should be managed on an individual basis depending on the clinical context. Here described is a case of a discrete nonatherosclerotic aneurysm of the left circumflex coronary artery in a 46-year-old man who presented with accelerated angina pectoris and was treated medically. The patient was free of symptoms on 2-year follow-up. The clinical perspectives of the nonatherosclerotic coronary aneurysm are discussed.

A left atrial paraganglioma patient presenting with compressive dysphagia.

Paragangliomas are rare neoplasms of neural crest origin arising in the chromaffin (pheochromocytoma) and chemoreceptor (chemodectoma) tissues. Only a few cases of paragangliomas have been reported in the heart. Most of the cardiac paragangliomas are located in, or adjacent to, the left atrium. The biological activity indicative of catecholamine production has rarely been shown in cardiac paragangliomas. Patients with cardiac paragangliomas may present with hypertension, or with various obstructive or compressive symptoms, depending on the location of the tumour. A left atrial paraganglioma compressing the esophagus causing dysphagia is presented. A 37-year-old female patient underwent work-up for dysphagia to solids. Transesophageal echocardiography showed the presence of a large mass in the dilated left atrium. The tumour was removed completely intact and was a benign noncatecholamine-secreting paraganglioma. The patient's dysphagia was relieved. The clinical perspectives of cardiac paraganglioma and cardiac dysphagia are discussed.

Painless limited dissection of the ascending aorta presenting with aortic valve regurgitation.

Aortic dissection is a medical emergency carrying high morbidity and mortality. Prompt diagnosis is sometimes difficult because of its varying presentations, but it is critical to the achievement of good clinical outcomes. This report describes 2 cases of painless aortic dissection that presented with aortic valve regurgitation. In both, the dissection was limited to the ascending aorta just distal to the aortic valve. These dissections were diagnosed by transthoracic and transesophageal echocardiography.

Relaxin promotes differentiation of human breast cancer cells MCF-7 transplanted into nude mice.

Previous studies showed that the hormone relaxin acts on human breast cancer MCF-7 cells in vitro by modulating cell proliferation and promoting cell differentiation toward a duct epithelial phenotype. The present study was designed to investigate whether relaxin retains these properties when acting in vivo on MCF-7 cell tumors developed in athymic nude mice. Mice bearing MCF-7 cell tumors transplanted under the mammary fat pad and estrogenized to sustain tumor growth were treated systemically with relaxin (10 microg/day) for 19 days. Vehicle-treated mice were used as controls. Thirty days later, the mice were sacrificed and tumor fragments were analyzed by light and electron microscopy and immunocytochemistry. Measurements of tumor volume were recorded weekly for the overall experimental period. The results obtained indicate that relaxin treatment promotes differentiation of tumor cells towards both myoepithelial-like and epithelial-like cells, as judged by the ultrastructural features of the cells and by the increased expression of smooth muscle actin and cadherins. Measurements of tumor size and of the number of cycling cells show that relaxin, at the doses and times of exposure used in this study, does not significantly influence tumor growth and cell proliferation.