Prior History Of Heart Disease Research Articles

Traumatic brain injury is not associated with significant myocardial dysfunction: an observational pilot study.

BackgroundMyocardial dysfunction has been well described with catastrophic neurological events, such as subarachnoid hemorrhage and brain death. There is very limited data describing myocardial function in the context of traumatic brain injury (TBI), as no prospective study has yet examined this association. The objective of our study was to evaluate cardiac function using echocardiography in patients with clinically important TBI.MethodsWe conducted a prospective observational study of consecutive TBI patients admitted to the intensive care unit. All patients older than 16 years with moderate to severe TBI according to the Glascow Coma Scale (GCS) were eligible for the study. Only patients with a prior history of heart disease or cardiomyopathy or evidence of brain death on admission were excluded. A complete transthoracic echocardiogram was performed within 4 days of admission.ResultsForty-nine patients (67 % males, median age 34 years) were included in the study. Forty-one patients had severe TBI (84 %) with a median GCS of six, 44 patients (90 %) required mechanical ventilation and 36 (74 %) intracranial pressure monitoring. Hospital mortality was 18 %. No patients had global left ventricular dysfunction as defined by a left ventricular ejection fraction (LVEF) below 50 % (95 % CI, 0–0.07). Average LVEF was 65 +/− 4 %. Four patients (8 %) had regional wall motion abnormalities with preserved LVEF.DiscussionThe main finding of this study is the absence of clinically significant myocardial dysfunction in patients with moderate or severe TBI. Although myocardial dysfunction has been well described in a variety of neurological settings, it is possible that the young age of TBI patients and the absence of cardiovascular risk factors are protective against significant myocardial injury from catecholamine excess.ConclusionsIn a group of patients with clinically important TBI, we did not identify any significant cardiac dysfunction.

The yield of routine pre-operative cardiovascular evaluation in stable patients scheduled for elective non-cardiac surgery

Preoperative cardiovascular evaluation is commonly performed in patients scheduled for non-cardiac surgery. The recent ACC/AHA guidelines provide an algorithm for such an evaluation but whether all patients scheduled for surgery would benefit from it is not known. We determined the yield of preoperative cardiovascular evaluation in 522 stable patients, with no prior history of heart disease, who were scheduled for elective non-cardiac surgery. There were 14 patients (2.7%) in which the cardiac consultant requested further testing pre-operatively, and in 5 of them (1%), the findings on cardiac consultation and further testing would be considered to have impacted the decision on performing the surgery or the long term outcome of the patients. Using multivariable logistic regression analysis, the only clinical variable predictive of further testing was age > 65 years (OR=4.47, p=0.001). The yield of preoperative cardiovascular evaluation in stable patients scheduled for non-cardiac surgery is relatively low. Further studies are needed to identify what subgroup of patients might benefit most from it and those in whom it might not be warranted.

Predictive factors of supraventricular arrhythmias after noncardiac thoracic surgery: a multicenter study.

Supraventricular cardiac arrhythmias are the most common rhythm disturbances in patients following thoracic surgery. The purpose of our study was to determine which of the clinical parameters are the most valuable in predicting postoperative atrial fibrillation (AF) after lung surgery. Retrospective analysis was carried out on 987 patients after noncardiac thoracic surgery to define the prevalence, associated risk factors, and clinical course of postoperative arrhythmias. There were 822 men and 165 women, age 34 to 78 years (mean age: 61 ± 8 years). The patients were divided into two groups depending on the occurrence or absence of supraventricular arrhythmia. Group I consisted of 876 patients who were free from rhythm disturbances. The remaining 111 patients exhibited episodes of supraventricular arrhythmia (29 supraventricular tachycardia; 82 AF). These 111 patients were placed in Group II. Preoperative, operative, and postoperative data were reviewed. Statistical analysis was performed. A statistically significant difference was found between the two groups in age, previous history of heart disease, and lung resection, especially pneumonectomy. Age, history of prior heart disease, lung resection, and the extent of pulmonary resection are the main risk factors for postoperative supraventricular arrhythmia in patients undergoing major thoracic operations.

PMM.09 Peripartum cardiomopathy – a case series

Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy that presents with signs of heart failure in the last month of pregnancy or within five months of delivery. It is...

Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Therapy Prescription in Men

BackgroundAn association between testosterone therapy (TT) and cardiovascular disease has been reported and TT use is increasing rapidly.MethodsWe conducted a cohort study of the risk of acute non-fatal myocardial infarction (MI) following an initial TT prescription (N = 55,593) in a large health-care database. We compared the incidence rate of MI in the 90 days following the initial prescription (post-prescription interval) with the rate in the one year prior to the initial prescription (pre-prescription interval) (post/pre). We also compared post/pre rates in a cohort of men prescribed phosphodiesterase type 5 inhibitors (PDE5I; sildenafil or tadalafil, N = 167,279), and compared TT prescription post/pre rates with the PDE5I post/pre rates, adjusting for potential confounders using doubly robust estimation.ResultsIn all subjects, the post/pre-prescription rate ratio (RR) for TT prescription was 1.36 (1.03, 1.81). In men aged 65 years and older, the RR was 2.19 (1.27, 3.77) for TT prescription and 1.15 (0.83, 1.59) for PDE5I, and the ratio of the rate ratios (RRR) for TT prescription relative to PDE5I was 1.90 (1.04, 3.49). The RR for TT prescription increased with age from 0.95 (0.54, 1.67) for men under age 55 years to 3.43 (1.54, 7.56) for those aged ≥75 years (ptrend = 0.03), while no trend was seen for PDE5I (ptrend = 0.18). In men under age 65 years, excess risk was confined to those with a prior history of heart disease, with RRs of 2.90 (1.49, 5.62) for TT prescription and 1.40 (0.91, 2.14) for PDE5I, and a RRR of 2.07 (1.05, 4.11).DiscussionIn older men, and in younger men with pre-existing diagnosed heart disease, the risk of MI following initiation of TT prescription is substantially increased.

Acute cardiogenic shock induced by infusional 5-Fluorouracil.

A 49-year-old patient with metastatic carcinoma of the bladder and no prior history of heart disease presented with diffuse ST elevation, elevated troponins, and biventricular dysfunction requiring intensive care unit admission and inotropic support after receiving her first course of infusional 5-fluorouracil (5-FU). Over the course of several days, the patient's cardiac function and clinical status returned to baseline. A follow-up echocardiogram performed 5 days after initial presentation revealed an ejection fraction of 59 percent, with no evidence of wall motion abnormalities. Subsequent 5-FU chemotherapy was discontinued, and the patient went on to receive second-line chemotherapy.

A Unique Case of Cardiac Arrest following K2 Abuse.

Sudden cardiac death (SCD) accounts for up to 450,000 deaths every year in the United States (Zipes et al. (2006)). Most cases of sudden cardiac death occur in subjects with no prior history of heart disease (Myerburg et al. (1998)). The incidence of sudden death in a general population has been shown to increase contemporaneously with substance abuse (Phillips et al. (1999)). The causative association of sudden death with cocaine, methadone, and volatile agents is well established (Adgey et al. (1995) and Isner et al. (1986)). We describe a case of out-of-hospital cardiac arrest temporally related to abuse of the synthetic cannabinoid street drug known as K2. To our knowledge, there are no previously documented cases of sudden cardiac death associated with synthetic cannabinoids although they have been linked to myocardial infarction in teenagers despite normal coronary angiography (Mir et al. (2011)).

Cardiac Troponin T as a Screening Test for Myocarditis in Children

The objective of this study was to define the test characteristics of cardiac troponin T (cTnT) in pediatric patients who presented with suspected myocarditis. We performed a retrospective cohort study of all patients at a large urban children's hospital 21 years or younger who had a cTnT test sent for evaluation for myocarditis over a 13-month period. Patients were excluded if they had any history of heart disease or cardiac arrest before presentation, or the cTnT was sent for reasons other than concern for myocarditis. Positive cases of myocarditis were defined by characteristic pathology findings, magnetic resonance imaging results, or diagnosis of the attending cardiologist at time of discharge. Six hundred fifty-two patients had cTnT sent during the study period. Two hundred sixty were excluded because of prior history of heart disease, and 171 had the test sent for reasons other than concern for myocarditis. Of the 221 patients included in the study, 49 had an initial positive cTnT (≥0.01 ng/mL), whereas 172 had a negative test result. Eighteen cases of myocarditis were identified. All patients with myocarditis had an elevated cTnT at presentation. Using a cutoff value of 0.01 ng/mL or greater as a positive test, cTnT had a sensitivity of 100% (95% confidence interval [CI], 78%-100%), with a negative predictive value of 100% (CI, 97%-100%), and a specificity of 85% (CI, 79%-89%), with positive predictive value of 37% (CI, 24%-52%), in the diagnosis of myocarditis. In children without preexisting heart disease, a cTnT level of less than 0.01 ng/mL can be used to exclude myocarditis.

Imatinib: the controversial discussion on cardiotoxicity induced by endoplasmic reticulum (ER) stress

The safety profile of imatinib, and especially its relevance to cardiotoxicity, has been controversially discussed in recent years (Kerkela et al. 2006; Herman et al. 2011; Wolf et al. 2010; Ribeiro et al. 2008). Therefore, the editors are pleased that Eirini Thanopoulou and Ian Judson from the Royal Marsden NHS foundation Trust in London contributed a comprehensive review on the long-term tolerability of imatinib (Gleevec) (Thanopoulou and Judson 2012). The introduction of imatinib represents one of the most prominent success stories in cancer therapy of the past decade. A reciprocal translocation creating the Philadelphia chromosome is involved in pathogenesis of more than 90% of the cases of chronic myelogenous leukaemia (CML) (Van Etten 2004). This translocation creates the Bcr-Abl fusion protein of the nonreceptor tyrosine kinase c-Abl and the multidomain protein Bcr, leading to a constitutively active cytosolic protein that activates several signalling pathways involved in proliferation and antiapoptosis. Imatinib inhibits the fusion protein, Bcr-Abl resulting in remission in a high fraction of patients with CML. In addition, imatinib is efficient in gastrointestinal stromal tumour (GIST), because—besides its effect on Bcr-Abl—it also inhibits KIT proteins that play a role in progression of GIST and other tumours (Joensuu et al. 2001; Micke et al. 2003, 2004). The success stories of imatinib, and the Her-2-targeting antibody, trastuzumab, led to the novel concept of identifying and targeting the mechanisms responsible of tumour progression, in addition to identifying subtypes of carcinomas with the perspective of a biologically justified therapy (Schmidt et al. 2008, 2010; Hellwig et al. 2010; Cadenas et al. 2010; Lee et al. 2010; Brase et al. 2010; Petry et al. 2010). Previously, Kerkela et al. (2006) reported on the cardiotoxic side effect of imatinib. Individuals without any prior history of heart disease developed heart failure after treatment with imatinib (Kerkela et al. 2006). Interestingly, imatinib also showed toxic effects on cultivated cardiomyocytes, most likely due to an induction of endoplasmic reticulum (ER) stress, leading to decreased translation and a block in protein synthesis (Kerkela et al. 2006). A simultaneous upregulation of stress response genes suggested that the ER stress response is an adequate mechanism to compensate short-term cell stress. However, prolonged activation may induce cell death by pathways, including Jun N-terminal kinases (JNKs), a mechanism shown for imatinib in cardiomyocytes (Kerkela et al. 2006). Since cardiotoxicity is one of the leading topics in toxicology addressed in our journal (Sumi et al. 2011; Vavrova et al. 2011; Lee et al. 2010), we welcome the current review by Thanopoulou and Judson (2012). Overall, imatinib shows an excellent long-term tolerability and the clinical relevance of imatinib-induced cardiotoxicity may have been overestimated. The comprehensive review of Thanopoulou and Judson (2012) comes highly recommended for anyone interested in the safety profile of imatinib.

Atrial fibrillation-induced cardiac shock: first manifestation of a congenitally corrected transposition of the great arteries in a 45-year-old man.

Background. The congenitally corrected transposition of the great arteries (L-TGA) is a very rare congenital heart defect, which often remains undetected for several decades of life. Case Presentation. We report on a 45-year-old man without prior history of heart disease, presenting with cardiac shock related to a first episode of tachycardic atrial fibrillation. The diagnostic work-up identified a L-TGA as the underlying cause for acute heart failure. Discussion. L-TGA is a very rare congenital heart defect, which is characterized by an atrioventricular as well as a ventriculoarterial discordance. By this means, the physiological sequence of pulmonary and systemic circulation is still maintained. On the basis of an ongoing strain of the right ventricle, which has to carry the burden of the systemic blood pressure, after more than four decades without symptoms, acute heart failure was triggered by a tachycardic atrial fibrillation.

Is There Still a Role for Preoperative 12‐Lead Electrocardiography?

Twelve-lead electrocardiography is a standard preoperative investigation for patients undergoing major surgery. There is uncertainty and debate over the usefulness of this test for stratifying postoperative cardiac risk. The aim of this study was to investigate the correlation between an abnormal electrocardiogram (ECG) and the postoperative cardiac event rate. A prospective single-center observational cohort study in patients undergoing major noncardiac surgery was performed. ECGs were analyzed at the end of the study by a cardiologist and a clinician blinded to the clinical outcomes. The primary endpoints were a major adverse cardiac event (MACE), defined as nonfatal myocardial infarction or cardiac death, and perioperative mortality. A total of 345 patients were included, who had undergone aortic surgery 25.8%, lower limb bypass 29.0%, amputation 25.2%, or laparotomy 20.0%. An abnormal ECG was present in 141 (40.9%) patients. MACE occurred in 46 (13.3%) cases. Patients with an abnormal ECG had a significantly higher incidence of MACE (21.6 vs. 8.3%, P < 0.001). Multivariate analysis showed that left ventricular strain and a prolonged QTc interval (>440 ms) were independent predictors of postoperative adverse events. Among patients with no prior history of ischemic heart disease, those with an abnormal ECG had a higher MACE rate (20.3%) than those patients with a normal ECG (8.6%) (P = 0.01). Preoperative electrocardiography is a useful screening test for predicting perioperative cardiac events. Patients with an abnormal ECG but without a prior history of heart disease are a high-risk group potentially amenable to intervention and risk reduction.

Terlipressin infusion induces Tako-Tsubo syndrome in a cirrhotic man with hepato-renal syndrome

Dr. Di Micoli, Dr. Buccione, Prof. Trevisani: TakoTsubo cardiomyopathy (TTC), also known as transient left ventricular apical ballooning syndrome, is a clinical entity characterized by (1) reversible left ventricular apical wall motion abnormalities, (2) typical electrocardiographic changes and (3) relatively minor elevation of troponine, creatinine-kinase (CK) and CK-MB that mimics an acute myocardial infarction (AMI) without any acute obstructive coronary disease [1]. Typically, the left ventricular imbalance almost always recovers in a period of days to weeks, so that the management and prognosis of this condition are clearly different from those of AMI [2]. TTC is generally observed in post-menopausal women without prior history of heart disease or clear risk factors for coronary artery disease, who have often experienced recent emotional or physical stress, non-cardiac surgery or extracardiac diseases [1]. Recently, TTC has also been described in critically ill patients without prior heart disease admitted to a medical intensive care unit for severe non-cardiac diseases, such as sepsis, acute respiratory failure, systemic inflammatory response syndrome, anaphylaxis and trauma injuries [3, 4]. Herein, we report a case of TTC occurring in a cirrhotic man, waiting for liver transplantation (LT), probably favored by the intravenous infusion of terlipressin, a synthetic analog of vasopressin (AVP), for the treatment of hepato-renal syndrome (HRS). A 67-year-old Caucasian man with hepatitis B virusrelated cirrhosis and ascites, waiting for LT, was admitted to our unit because of the onset of hepatic encephalopathy, and the worsening of renal sodium retention. As a candidate for LT, he had undergone clinical, laboratory and instrumental tests aimed at excluding extrahepatic diseases precluding surgery. Myocardial single photon emission computed tomography had excluded ischemic damage, and trans-thoracic echocardiography had ruled out dyskinesia of ventricular segments and documented a normal (65%) left ventricular ejection fraction (LVEF). On admission, the patient presented with peripheral edema, ascites and grade III hepatic encephalopathy. Daily diuresis was around 200 mL. The ongoing therapy included oral diuretics (furosemide 25 mg b.i.d. and spironolactone 100 mg b.i.d.), lamivudine and tenofovir for HBV infection control, norfloxacine (400 mg/day) for secondary prophylaxis of the spontaneous peritoneal peritonitis, lactulose, and periodic albumin infusion. The serum creatinine was 2.2 mg/dL and blood urea nitrogen 0.9 g/dL, while serum electrolyte concentrations were normal (sodium 138 mEq/L, potassium 3.5 mEq/L, calcium 8.9 mg/dL and magnesium 2.6 mEq/L). The hemoglobin level was 10.4 g/dL, platelet count 134.000/lL, leukocytes 8.0 9 10/mmc, serum bilirubin 18.8 mg/dL, albumin 3.4 g/dL, INR 2.11. A. Di Micoli D. Buccione V. Santi L. Bastagli M. Bernardi F. Trevisani Dipartimento di Medicina Clinica, Alma Mater Studiorum-Universita degli Studi di Bologna, Bologna, Italy

Clinical Significance of Cardiac Co-Morbidities and Risk Factors for Patients Treated with Imatinib.

AbstractAbstract 4490 Background:Imatinib is currently standard therapy for patients with success in Chronic Myeloid Leukemia (CML). Several instances of cardiac adverse events have been reported for patients while on therapy with imatinib. In many instances, these events occur in patients with pre-existing cardiac conditions. The aim of our study was to determine the occurrence of cardiac events in patients with CML treated with Imatinib, and the impact that cardiac risk factors and pre-existing cardiac conditions had on the risk of developing cardiac adverse effects. Methods:We reviewed the medical records of 51 patients with chronic phase CML who were treated with imatinib after failing prior therapies. For each patient we collected cardiac risk factors, pre-existing cardiac disease, pre-treatment EKG and echocardiogram (ECHO) readings, as well as post-treatment changes in EKG and ECHO findings. Results:Pre-existing cardiac conditions were found in 14 (27%) patients, including congestive heart failure in 2 (4%), myocardial infarction in 4 (8%), atrial fibrillation in 1 (2%), benign arrhythmias in 1(2%), aortic regurgitation in 1(2%), mitral valve prolapse in 1 (2%), mitral regurgitation in 1(2%), pericarditis in 1(2%), bradycardia in1(2%) and benign arrhythmia in 1(2%). Cardiac risk factors were present in 26 patients (51%), including smoking in 10 patients (20%), hypertension in 17 (33%), diabetes mellitus in 9 (18%), obesity in 2 (4%), hyperlipidemia in 5 (10%), stress (self-reported by patient or on anxiolytic therapy) in 5 (10%), alcohol in 11 (22%), atherosclerosis in 3 (6%), and positive family history for cardiac disease in 5 patients (9.8%). Cardiac events were noted in 19 patients (37%) of whom 11 (58%) had pre-existing cardiac conditions prior to initiating imatinib treatment and 14 patients (27%) had at least one cardiac risk factor. Congestive heart failure with clinical manifestations was seen in 9 patients (18%) with documentation of decreased ejection fraction on echocardiogram seen in 3 patients (6%) who had a decrease in LVEF from a median of 55% (range 50% to 72%) to a median of 45% (range 25% to 60%). Out of the patients who developed CHF while on treatment with imitanib, 3 patients (6%) had history of cardiac conditions (atrial fibrillation in 1 (2%), congestive heart failure in 2 (4%)). Myocardial infarction was documented in 3 patients (6%), one of which had prior myocardial infarction and pacemaker, another had history of mitral valve prolapse and hypertension; one patient had hypertension, diabetes mellitus and positive family history but no prior history of heart disease. Arrhythmia was seen in 3 patients (6%). Post-treatment EKG changes occurred in 14 patients (27%) including bradycardia, PAC's, PVC's, ST-T wave changes, tachycardia and other rhythm abnormalities. These changes were usually asymptomatic. Gated cardiac study done after a median of 63 months (range 29 to 83 months) after initiation of imatinib treatment showed EF below 60% in 9 patients (18%) with a median of 55% (range 36% to 59%). None of the patients died of cardiac conditions and none discontinued imatinib therapy because of cardiac events. Conclusion:Although cardiac events occur in some patients treated with imatinib, these are much more common among patients with pre-existing cardiac conditions and/or cardiac risk factors. These patients need to be monitored closely to minimize their risk and intervene early when new cardiac events arise. Disclosures:Cortes:novartis: Research Funding; BMS: Research Funding; Pfizer: Consultancy, Research Funding. Kantarjian:novartis: Research Funding; BMS: Research Funding. O'Brien:Novartis: Research Funding.

Prevalence Of Diastolic Dysfunction And Association With Peak Vo2 In Obese Patients Without History Of Heart Disease

PURPOSE: Diastolic dysfunction (DD) can cause increased pressure und fluid in the blood vessel of the lung which might lead to dyspnea on exertion. Moreover, dyspnea is a common symptom in obese patients. Thus, we sought to evaluate the prevalence of DD in obese patients and to assess whether obese patients with DD have a reduced peak VO2. METHODS: 92 consecutive obese patients (22 female, mean age 42 ±11.7 years [18-70], mean BMI 44.3 ± 8.6 kg/m2 [30.0-74.7]) with normal systolic left ventricular function were included in this study. All patients were evaluated by echocardiography prior to incremental treadmill exercise testing using a walking protocol to determine peak VO2. Diastolic dysfunction was defined as an inversed E/A-ratio derived from transmitral valve flow pattern. RESULTS: DD was observed in 35/92 patients (38%). Mean peak VO2 was 20.2 ± 4.6 mL/kg/min [10-31] with a significant high value in patients with normal diastolic function (21.0 ± 4.8 mL/kg vs. 18.9 ± 4.1 mL/kg, p<0.05). However, after adjustment for age, gender and body mass index, this difference was no longer significant. CONCLUSIONS: Diastolic dysfunction is common in obese patients without history of prior heart disease. However, in a multifactorial model the presence of diastolic dysfunction was not associated with reduced peak VO2 as assessed by treadmill test. Thus, dyspnea in obese patients with diastolic dysfunction might not be explained by a reduced peak VO2.

Optimizing Survival from Out‐of‐Hospital Cardiac Arrest

Cardiac arrest is an important public health problem and often occurs in the out-of-hospital setting in patients without a prior history of heart disease. Very few communities or emergency medical service (EMS) systems report survival rates for out-of-hospital cardiac arrest. Among those who do, survival rates vary substantially between cities, due in large part to community differences in the chain of survival. To improve survival in cardiac arrest, care must be optimized at each point along the cardiac arrest continuum, including a rapid emergency response, provision of cardiopulmonary resuscitation (CPR) by bystanders, delivery of high-quality chest compressions with minimal interruptions by first responders, rapid defibrillation, and optimization of postresuscitation care, including therapeutic hypothermia. Important current initiatives to improve cardiac arrest survival include hands-only CPR delivered by laypersons prior to the arrival of EMS, dispatcher-assisted CPR, and implementation of hospital-based therapeutic hypothermia protocols to improve postresuscitation care. Optimizing cardiac arrest survival requires a team effort between EMS directors, emergency physicians, cardiologists, hospital leadership, and the public.

Could Beta Blockade Improve Outcome After Injury by Modulating Inflammatory Profiles?

Cardioprotection with beta-receptor antagonists improves outcome in high risk patients undergoing elective surgery. Recent trials have demonstrated an association between beta blocker (BB) use and improved outcomes after injury. The mechanisms through which BB result in improved outcomes remain poorly elucidated. In vitro evidence supports that BB modulates the postinjury inflammatory response. The purpose of this study was to examine the effects of BB on inflammatory profiles in injured patients at increased risk for heart disease. A pseudo-randomized, controlled trial of injured patients over 55 admitted to the intensive care unit was conducted. Patients were randomized to receive continuous BB or standard of care. Patients with a reported history of prehospital BB use were enrolled into an observational arm of the trial, continued on BB, and analyzed with the continuous BB group. Plasma interleukin (IL)-6 and IL-1beta levels were measured by enzyme-linked immunosorbent assay at baseline and day 1, 2, and 4 after BB initiation. Cytokine data were log transformed for normality assumptions. Repeated measures analysis of variance was used to test for within-group differences in cytokine levels over time. Forty-two patients were enrolled. Seventeen patients were randomized to the control group and 25 patients received continuous BB (10 randomized/15 observational). There was no difference in gender, age, prior history of heart disease, or admission heart rate, systolic blood pressure or initial base deficit between groups. Baseline levels of IL-6 and IL-1beta did not differ between groups. Levels of IL-6, but not IL-1beta, decreased over time in patients receiving BB (p = 0.04), whereas levels in controls remained unchanged (p = 0.27). There were no BB related complications. Use of BB decreases serum IL-6 levels over time in injured patients at risk for heart disease. This may contribute to improved outcomes noted in trauma patients receiving BB. Additionally, BB use in this population of patients is safe after endpoints of resuscitation have been met.

Radiation Therapy, Cardiac Risk Factors, and Cardiac Toxicity in Early-Stage Breast Cancer Patients

The benefits of adjuvant radiation therapy (RT) for breast cancer may be counterbalanced by the risk of cardiac toxicity. We studied the cardiac effects of RT and the impact of pre-existing cardiac risk factors (CRFs) in a population-based sample of older patients with breast cancer. In the Surveillance, Epidemiology and End-Results (SEER)-Medicare database of women > or = 65 years diagnosed with Stages I to III breast cancer from January 1, 1992 to December 31, 2000, we used multivariable logistic regression to model the associations of demographic and clinical variables with postmastectomy and postlumpectomy RT. Using Cox proportional hazards regression, we then modeled the association between treatment and myocardial infarction (MI) and ischemia in the 10 or more years after diagnosis, taking the predictors of treatment into account. Among 48,353 women with breast cancer; 19,897 (42%) were treated with lumpectomy and 26,534 (55%) with mastectomy; the remainder had unknown surgery type (3%). Receipt of RT was associated with later year of diagnosis, younger age, fewer comorbidities, nonrural residence, and chemotherapy. Postlumpectomy RT was also associated with white ethnicity and no prior history of heart disease (HD). The RT did not increase the risk of MI. Presence of MI was associated with age, African American ethnicity, advanced stage, nonrural residence, more than one comorbid condition, a hormone receptor-negative tumor, CRFs and HD. Among patients who received RT, tumor laterality was not associated with MI outcome. The effect of RT on the heart was not influenced by HD or CRFs. It appears unlikely that RT would increase the risk of MI in elderly women with breast cancer, regardless of type of surgery, tumor laterality, or history of CRFs or HD, for at least 10 years.

A case of acute myocardial infarction during 5-fluorouracil infusion

Cardiac toxicity is an uncommon side-effect of 5-fluorouracil (5-FU) treatment, consisting mainly of chest pain episodes with or without electrocardiographic changes and dysrhythmias. Here, we describe the case of a 56-year-old male patient with a diagnosis of advanced colorectal cancer who developed an acute myocardial infarction during 5-FU infusion. The patient was not affected by prior heart disease and did not show any classic risk factors for coronary heart disease. Coronary angiography examination revealed no evidence of coronary stenosis, supporting the hypothesis of a coronary artery spasm related to 5-FU infusion. Given the great number of cancer patients receiving 5-FU containing chemotherapeutic regimens, this rare but severe cardiac side-effect may be observed in both cardiologic and oncologic clinical practice. We suggest a tight clinical monitoring of all patients receiving 5-FU infusions, even in those without a prior history of heart disease.

Architecture of Intracoronary Thrombi in ST-Elevation Acute Myocardial Infarction

Patient 1, a 46-year-old man, and patient 2, a 53-year-old man, both current smokers, were admitted to our center 60 minutes and 6 hours, respectively, after the onset of a first episode of ST-elevation inferior wall acute myocardial infarction. Neither of the patients had a prior history of heart disease or any risk factor for coronary artery disease other than a history of smoking. Both underwent coronary angiography with a transradial approach, revealing single-vessel disease consisting of a TIMI grade 0 occlusion of the proximal right coronary artery (Figure 1A and Figure 2A). Both patients received 500 mg IV aspirin, 300 mg …

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD)

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD). Cardiovascular calcification (CVC) is commonly encountered both in the general population as well as in patients with end-stage renal disease (ESRD). The etiology of CVC in patients with ESRD is multifactorial. Despite that, current debate remains narrowly focused on the role of calcium loading from calcium-based phosphate binders (CBPB) in the pathogenesis and progression of CVC. Yet, the alleged link between these binders and CVC has not been substantiated in well-designed controlled trials. In contrast, the purported role of sevelamer, a non-calcium-based phosphate binder, in slowing the progression of CVC in dialysis patients has attracted widespread attention. The beneficial effect of sevelamer on progression of calcification was thought to be due to lower calcium loading during its use. However, an alternative and possibly more likely mechanism involves sevelamer-induced lowering of LDL cholesterol. In this context, previous studies in individuals with normal renal function have documented amelioration of coronary artery calcification (CAC) with reduction of LDL-cholesterol by treatment with HMG-CoA reductase inhibitors (statins). Given that CAC is a well-accepted marker of atherosclerosis, and that high plasma cholesterol concentration is one of the main risk factors for atherosclerosis, then it is not unreasonable to suspect that CAC may be halted or even reversed by lowering of LDL cholesterol level with statin therapy. Unfortunately, the effect of lowering the LDL-cholesterol level on CAC has not been studied in patients with ESRD. Therefore, conclusions about this important topic should await the results of well-designed clinical studies that control for all factors potentially implicated in the CVC burden of patients with ESRD. In this review, I will discuss the role of various potential mechanisms involved in the pathogenesis of CVC in patients with ESRD, and emphasize the role of dyslipidemia and its treatment in this important clinical entity.