Late Cardiac Complications Research Articles

Number of erythrocyte transfusions is more predictive than serum ferritin in estimation of cardiac iron loading in pediatric patients with acute lymphoblastic leukemia

BackgroundTransfusions with packed erythrocytes is a common practice in pediatric patients with acute lymphoblastic leukemia (ALL) who are on chemotherapy. Since there is no physiological excretion mechanism for iron, the iron related to erythrocyte transfusions accumulates and may contribute to late cardiac, hepatic and endocrine complications in these patients. ProcedureIn order to evaluate the iron burden among pediatric patients with ALL and define the risk factors associated with higher iron loading, we evaluated 79 pediatric patients with ALL (36 were off-therapy). Cardiac and hepatic T2* were ordered to a total of 22 (28%) patients who were either transfused with erythrocytes ≥10 times (n=11; 50%), had serum ferritin (SF) ≥1000ng/ml (n=2; 9.1%) or both (n=9; 40.9%). ResultsHalf of the patients who were screened by T2* MRI had hepatic T2*<7ms and six (27%) of the patients had cardiac T2*<20ms, indicating iron loading. Patients who had serum ferritin <1000 vs ≥1000ng/ml had median cardiac T2* values of 28.3ms (15–40) vs 21 (7.9–36), (p=0.324); whereas hepatic T2* of 10.8 (5.32–27) vs 4.7 (2.2–36), (p=0.017). Patients who had erythrocyte transfusion <10 vs ≥10 times had median cardiac T2* values of 34ms (28–38) vs 23 (7.93–40), (p=0.021); whereas hepatic T2* of 13.6 (6.6–36) vs 5.32 (2.2–27), (p=0.046). ConclusionsOur results indicate that pediatric patients with ALL should be screened for transfusional iron load and the amount of erythrocyte transfusions seems to be a more reliable indication than serum ferritin levels to detect cardiac iron loading in these patients.

Are cardiac Magnetic Resonance Imaging and Radionuclide Ventriculography Good Options Against Echocardiography for Evaluation of Anthracycline Induced Chronic Cardiotoxicity in Childhood Cancer Survivors?

Anthracyclines are widely used for the treatment of solid tumors in pediatric oncology. However, their uses may be limited by progressive chronic cardiotoxicity related to the cumulative dosage. The aims of this study are to compare diagnostic techniques and prepare an algorithm for diagnosis of anthracycline induced chronic cardiotoxicity. The patients were evaluated according to age, sex, time elapsed since the last dose of anthracycline treatment, presence of cardiovascular symptoms, follow-up duration, type of anthracycline, cumulative anthracycline dose, and concomitant mediastinal radiation therapy. Late subclinical cardiotoxicity was detected by history, physical examination, electrocardiography (ECG), Holter monitor, echocardiography (ECHO), radionuclide ventriculography (MUGA), and cardiac magnetic resonance imaging (MRI). Thirty-seven male and 19 female patients with a median age of 11.2 ± 4.6 (range, 3.5–22.0) years were included in the study. Patients were grouped according to cumulative anthracycline doses. Subclinical cardiac dysfunction was detected in 20 patients by at least one of ECHO, MRI or MUGA after anthracycline chemotherapy. We revealed that other than ECHO, MRI and MUGA have high clinical importance for evaluating subclinical late cardiac complications in children treated with anthracyclines.

Undetected Aorto-RV Fistula With Aortic Valve Injury and Delayed Cardiac Tamponade following a Chest Stab Wound: A Case Report

IntroductionAlthough a few patients will survive after penetrating cardiac injuries, some of them may have unnoticeable intracardiac injuries. The combination of aorto-right ventricular fistula with aortic valve injury is rare.Case PresentationA 19 year-old man referred with an aorto-right ventricular fistula accompanied with aortic regurgitation and delayed tamponade following a stab in the chest. The patient was scheduled for fistula repair, aortic valve replacement and pericardectomy two months after trauma.ConclusionsTo prevent missing intracardiac injury and also late cardiac injury complications, in all pericordial stab wounds, serial clinical examinations and serial echocardiography should be performed. In addition, cardiac injuries should be repaired during the same hospital stay.

Growth-differentiation factor-15 and tissue doppler ımaging in detection of asymptomatic anthracycline cardiomyopathy in childhood cancer survivors

ObjectivesAnthracyclines have led to an increased risk of cardiac morbidity and mortality. Late cardiac complications in cancer survivors may develop from subclinical myocardial damage. Tissue Doppler imaging (TDI) also has potential as a clinically useful technique for the assessment of myocardial function. Biochemical markers may be used to detect cardiac damage growth-differentiation factor-15 (GDF-15) and are emerging as a biomarker of cardiac dysfunction. The aim of this study is to assess the value of the plasma levels of GDF-15 and TDI in detecting late myocardial dysfunction in childhood cancer survivors (CCS) who were treated with anthracyclines. Design and methodsThirty-eight CCS who had completed chemotherapy treatment with anthracyclines were included in this study. Control group consisted of 32 age- and gender-matched healthy volunteers. All children underwent a detailed echocardiography, which contained an M-mode, pulse Doppler and tissue Doppler imaging. However, GDF-15 and cardiac troponin-I (cTnI) were measured. ResultsAlthough, systolic function of the left ventricular was similar in all groups, there were significant differences between parameters of diastolic function of the heart. The mitral valve E wave, E/A ratio, left ventricular E′m wave, and E′m/A′m ratio were different in the patients than in the controls (p=0.049, p=0.037, p<0.0001, p=0.001, respectively). The tricuspid valve E/A ratio, right ventricular E′t wave, and E′t/A′t ratio in the patients were also different from those of the controls (p=0.031, p<0.0001, p<0.0001, respectively). Mean plasma GDF-15 was significantly higher in patients than healthy controls (p=0.027). There were no significant differences in cTnI between both groups. ConclusionsGrowth-differentiation factor-15 level may be used as a biomarker of anthracycline-induced cardiovascular disease severity in the CCS.

Two novel and functional DNA sequence variants within an upstream enhancer of the human NKX2-5 gene in ventricular septal defects

Mortality in patients with congenital heart disease (CHD) is significantly increased even with successful surgeries. The main causes are late cardiac complications, such as heart failure and arrhythmia, probably due to genetic defects. To date, genetic causes for CHD remain largely unknown. NKX2-5 gene encodes a highly conserved homeobox transcription factor, which is essential to the heart development in embryos and cardiac function in adults. Mutations in NKX2-5 gene have been implicated in diverse types of CHD, including ventricular septal defect (VSD). As NKX2-5 is a dosage-sensitive regulator, we have speculated that changed NKX2-5 levels may mediate CHD development by influencing cardiac gene regulatory network. In previous studies, we have analyzed the NKX2-5 gene promoter and a proximal enhancer in VSD patients. In the present study, we further genetically and functionally analyzed an upstream enhancer of the NKX2-5 gene in large cohorts of VSD patients (n=340) and controls (n=347). Two novel heterozygous DNA sequence variants (DSVs), g.17483576C>G and g.17483564C>T, were identified in three VSD patients, but none in controls. Functionally, these two DSVs significantly decreased the activity of the enhancer (P<0.01). Another novel heterozygous DSV, g.17483557Ins, was found in both VSD patients and controls with similar frequencies (P>0.05). Taken together, our data suggested that the DSVs within the upstream enhancer of the NKX2-5 gene may contribute to a small number of VSD. Therefore, genetic studies of CHD may provide insight into designing novel therapies for adult CHD patients.

Delay in diagnosis of Churg–Strauss syndrome: a case report

Churg-Strauss syndrome (CSS) is a well established disorder of the blood vessels. However, it is still sometimes not diagnosed early enough to avoid serious complications. It is the later stage that carries the more serious complications. Therefore, we emphasize the ways in which the diagnosis can be made early enough to avoid this stage of the disease. We report a case of CSS that was not diagnosed early and so the patient went on to develop severe cardiac and neurological manifestations. In this report we discuss the techniques and the methods to diagnose CSS and discuss their effectiveness in establishing the diagnosis. We also explore late cardiac and neurological complications because these are particularly serious complications later in the disease. We conclude that the criteria established by the American College of Rheumatology for CSS is the best tool available for early diagnosis and that late stage manifestations of CSS carry high rates of morbidity and mortality.

Genetic analysis of the TBX1 gene promoter in ventricular septal defects

Congenital heart disease (CHD) is the most common birth defects in humans. The genetic causes for CHD remain largely unknown. T-box transcription factor 1 (TBX1), a dosage-sensitive regulator, plays a critical role in the heart development. Mutations in the coding regions of TBX1 gene have been associated to 22q11 deletion syndrome with cardiac defects and isolated CHD cases, including ventricular septal defect (VSD). To date, TBX1 gene promoter region has not been analyzed and reported in CHD patients. We hypothesized that the sequence variants within TBX1 gene promoter region may change TBX1 levels and mediate CHD development. In this study, the promoter regions of TBX1 gene were genetically and functionally analyzed in 280 VSD patients and 267 healthy controls. Two novel heterozygous variants, g.4353C>T and g.4510A>C, were found in two VSD patients, but in none of controls. The single-nucleotide polymorphism-rs41260844, g.4199T>C, was found more frequent in VSD patients than controls (P < 0.01). Functional analyses revealed that these sequence variants significantly enhanced transcriptional activities of TBX1 gene promoter. Therefore, the sequence variants within TBX1 gene promoter may contribute to the VSD etiology by altering the expression levels of TBX1 gene. Pharmaceutical or genetic manipulation of TBX1 gene expression may provide a novel personalized therapy to prevent and treat late cardiac complications for the adult CHD patients carrying these variants.

Genetic and Functional Analysis of the NKX2-5 Gene Promoter in Patients With Ventricular Septal Defects

The ventricular septal defect (VSD) is the most common type of congenital heart disease (CHD). The morbidity and mortality of CHD patients are significantly higher due to late cardiac complications, likely caused by genetic defects. Mutations in cardiac transcription factor genes such as GATA-4, TBX5, and NKX2-5 have been implicated in CHD cases. The NKX2-5 gene, a homeobox gene, is expressed in the developing heart and the adult heart. Because NKX2-5 is a dosage-sensitive regulator during embryonic development, the authors hypothesized that the expression levels of the NKX2-5 gene rather than the mutant protein may play important roles in CHD. In this study, the promoter regions and exon regions of the NKX2-5 gene were bidirectionally sequenced in large cohorts of VSD patients and healthy control subjects. The results showed that a novel sequence variant (g.4574c>deletion), found only in one VSD patient, and a single nucleotide polymorphism (rs118026695), the frequency of which was significantly higher in VSD patients, were identified within the promoter region. Functional analysis confirmed that these sequence variants significantly enhanced the transcriptional activities of the NKX2-5 gene promoter, altering the expression of the NKX2-5 gene and the cardiac gene regulatory network. In addition, a synonymous mutation in the second exon of the NKX2-5 gene was identified in one VSD patient, which may affect the translation process. Therefore, the authors' data provide supportive evidence that mutations in the coding region of the NKX2-5 gene and sequence variants within its promoter region may be among the contributors to the CHD etiology.

Evaluation of dose to cardiac structures during breast irradiation.

Adjuvant radiotherapy for breast cancer can lead to late cardiac complications. The highest radiation doses are likely to be to the anterior portion of the heart, including the left anterior descending coronary artery (LAD). The purpose of this work was to assess the radiation doses delivered to the heart and the LAD in respiration-adapted radiotherapy of patients with left-sided breast cancer. 24 patients referred for adjuvant radiotherapy after breast-conserving surgery for left-sided lymph node positive breast cancer were evaluated. The whole heart, the arch of the LAD and the whole LAD were contoured. The radiation doses to all three cardiac structures were evaluated. For 13 patients, the plans were acceptable based on the criteria set for all 3 contours. For seven patients, the volume of heart irradiated was well below the set clinical threshold whereas a high dose was still being delivered to the LAD. In 1 case, the dose to the LAD was low while 19% of the contoured heart volume received over 20 Gy. In five patients, the dose to the arch LAD was relatively low while the dose to the whole LAD was considerably higher. This study indicates that it is necessary to assess the dose delivered to the whole heart as well as to the whole LAD when investigating the acceptability of a breast irradiation treatment. Assessing the dose to only one of these structures could lead to excessive heart irradiation and thereby increased risk of cardiac complications for breast cancer radiotherapy patients.

Cause-Specific Conditional Survival In 2603 Consecutive Patients Undergoing Autologous Hematopoietic Cell Transplantation (aHCT) Over a 20-Year Period

AbstractAbstract 933 Background:aHCT is offered with curative intent to patients with hematologic malignancies. However, survival estimates are conventionally computed from time of transplantation. These estimates provide initial prognosis, but do not reflect how prognosis changes with changing hazard rates over time. Conditional survival accounts for elapsed time since diagnosis, describing the probability of survival after having already survived a certain period of time after aHCT. We describe cause-specific conditional survival, providing clinically relevant information to inform preventive and interventional strategies for patients alive for differing lengths of time from aHCT. Methods:From 1986 to 2006, a total of 2,603 consecutive patients received aHCT at City of Hope at a median age of 48 yrs (NHL: n=1063; MM: n=625; HL: n=475; AML: n=330; other: n=110). Information regarding vital status and cause of death were determined using National Death Index Plus and medical records. Survival probabilities and standardized mortality ratios (SMRs) were calculated for the entire cohort as well as by diagnosis, conditional on survival for 1, 2, 5, and 10 yrs after aHCT. Results:A total of 1135 deaths (representing 44% of the cohort) were observed by December, 2007; 79% of deaths were attributed to recurrent disease (range: 88% after MM to 71% after HL); 8% to subsequent neoplasm (SMN: range: 4% after MM to 13% after HL); 6% to cardiopulmonary disease (range: 2% after MM to 10% after HL); and 7% to other causes. Using conventional survival estimates, overall survival (OS) was 60% at 5 yr and 48% at 10 yr from aHCT; and the cohort was at a 15.6-fold increased risk of premature death compared with the general population (95%CI=14.7-16.6). Females were at a higher risk of premature death (SMR=19.1) than males (SMR=12.3). The cohort was at a 4.9-fold (95%CI=3.9-5.9) increased risk of death due to SMNs, and at a 2.3-fold (1.5-3.2) increased risk of deaths due to late cardiac complications. Conditional survival estimates demonstrated that every additional yr survived was associated with an increase in the probability of surviving the subsequent 5 yrs. Thus, the 5-yr survival rate was 68% after surviving 1 yr, 73% after surviving 2 yr, 80% after 5 yr; and approaching 88% after having survived 10 yrs from aHCT (Figure). Cause-specific conditional survival rates and SMRs by primary diagnosis are summarized in the Table. The risk of premature death (due to any cause) was comparable to the general population for 10-yr survivors, with the exception of HL survivors (2.6-fold increased). With the exception of MM, individuals who had survived 10 years were projected to have a <5% risk of relapse-related mortality over the next 5 yrs (range: AML – 0% to HL: 5%). However, non-relapse mortality remained elevated long-term, indicating a need for extended surveillance. Conclusion:This study demonstrates that the projected 5-yr survival rates improve conditional on previous time survived from aHCT, and that the 10-year survivors of aHCT for AML, NHL, and MM have mortality rates that are comparable to the general population. HL survivors continue to experience a 2.6-fold increased risk of premature death, primarily because of the excess risk of non-relapse mortality (due to SMN and cardiac causes). Conditional survival estimates provide clinically relevant prognostic information and an accurate estimate of cause-specific survival, helping inform preventive and interventional strategies.TableCause-specific Conditional Survival in patients undergoing autologous HCTfrom aHCT1 yr survivors5 yr survivors10 yr survivors5 yr survivorsSMR (95%CI)5 yr survivorsSMR (95%CI)5 yr survivorsSMR (95%CI)5 yr survivorsSMR (95%CI)All patientsOverall6015.6(14.7–16.5)689.5(8.8–10.2)803.5(3.0–4.1)881.5(1.0–2.0)Relapse-related65748897Non-relapse-related92939291AMLOverall6215.7(13.1–18.3)748.8(6.8–10.8)862.8(1.4–4.0)911.1(0.02–2.1)Relapse-related647694100Non-relapse-related96999391NHLOverall6114.0(12.7–15.2)747.2(6.3–8.1)813.0(2.3–3.7)861.4(0.7–2.1)Relapse-related66809298Non-relapse-related92938988HLOverall5930.4(26.3–34.5)6619.4(16.1–22.7)846.5(4.4–8.5)902.6(0.9–4.3)Relapse-related68769195Non-relapse-related87889295MMOverall5910.9(9.5–12.3)569.1(7.8–10.3)633.8(2.6–4.9)841.1(0–2.6)Relapse-related63606684Non-relapse-related959595100 [Display omitted] Disclosures:Nademanee:Genzyme: Consultancy, Research Funding; Allos Therapeutics: Membership on an entity's Board of Directors or advisory committees; Spectrum Pharmaceuticals: Membership on an entity's Board of Directors or advisory committees.

From Creatine Kinase-MB to Troponin

From Creatine Kinase-MB to Troponin

Long-term cardiac effects of treatment for childhood leukemia

Late cardiac complications in cancer survivors may develop from subclinical myocardial damage. Biochemical correlates of minimal myocardial changes can be analyzed using a commercially available rapid assay. Biomarkers are considered more sensitive markers of subclinical cardiotoxicity than conventional electrocardiographic and echocardiographic methods. The aim of this study was to determine the values of plasma N-terminal pro brain natriuretic peptide (NT-pro-BNP) and cardiac troponin T (cTnT) in asymptomatic childhood leukemia survivors after anthracycline therapy in comparison with healthy volunteers. The survivors also underwent a detailed echocardiography. Twenty six survivors of leukemia previously treated with anthracyclines with total cumulative dose 95-600 (median 221) mg/m(2) were evaluated. Analyses of cTnT and NT-proBNP from blood samples and echocardiography were performed 5-25 years after completion of therapy for childhood leukemia. Control group for biochemical analyses consisted of 22 age- and gender- matched apparently healthy volunteers. Values of NT-proBNP were significantly elevated in ANT group compared to controls (35.1 +/- 37.8 vs. 9.6 +/- 6.7 pg/ml, P<0.010). CTnT remained below the diagnostic cut-off values in both groups. All echocardiographic parameters of patients remained normal. In conclusion, differences in NT-proBNP values between patients treated with anthracyclines and healthy volunteers might signal an initial stage of anthracycline-induced myocardial damage. The potential of this biomarker to detect subclinical anthracycline-induced myocardial alterations before development of echocardiographic and clinical changes is promising.

Using surface imaging and visual coaching to improve the reproducibility and stability of deep-inspiration breath hold for left-breast-cancer radiotherapy

Late cardiac complications may arise after left-breast radiation therapy. Deep-inspiration breath hold (DIBH) allows reduction of the irradiated heart volume at the same time as it reduces tumor bed motion and increases lung sparing. In the present study, we have evaluated the improvement in reproducibility and stability of the DIBH for left-breast-cancer treatment when visual coaching is provided with the aid of 3D video surface imaging and video goggles. Five left-breast-cancer patients and fifteen healthy volunteers were asked to perform a series of DIBHs without and with visual coaching. Reproducibility and stability of DIBH were measured for each individual with and without visual coaching. The average reproducibility and stability changed from 2.1 mm and 1.5 mm, respectively, without visual feedback to 0.5 mm and 0.7 mm with visual feedback, showing a significant statistical difference (p < 0.001 for reproducibility, p < 0.01 for stability). Significant changes (>2 mm) in reproducibility and stability were observed in 35% and 15% of the subjects, respectively. The average chest wall excursion of the DIBH with respect to the free breathing preceding the DIBH was found to be 11.3 mm. The reproducibility and stability of the DIBH improve significantly from the visual coaching provided to the patient, especially in those patients with poor reproducibility and stability.

Escalation and Intensification of Radiotherapy for Stage III Non-small Cell Lung Cancer: Opportunities for Treatment Improvement

In this overview we review and model how radiotherapy tumour control and complication rates vary with dose, fractionation, schedule duration, irradiated volume and use of chemotherapy for stage III non-small cell lung cancer (NSCLC), and use the modelling to study the effectiveness of different NSCLC dose-escalation approaches being developed in the UK. Data have been collated for pneumonitis, lung fibrosis, early and late oesophagitis, cord and cardiac complications, and local progression-free survival at 30 months. Dependences of the various end points on treatment-related factors are catalogued and analysed using the linear-quadratic incomplete repair model to account for dose and fractionation effects, making linear corrections for differences in schedule duration, and loosely characterising volume effects using parallel- and series-type concepts. Tolerance limits are calculated for the different end points and distilled into ranges of prescribed dose likely to be tolerable when delivered in 2.5 and 4 week radiation and 6 week chemoirradiation schedules using conformal techniques. Worthwhile (∼20%) gains in 30 month local progression-free survival should be achievable at safely deliverable levels of dose escalation. The analysis suggests that longer schedules may be more beneficial than shorter ones, but this finding is governed by the relative rates of tumour and oesophageal accelerated proliferation, which are quite imprecisely known. Consequently escalated 2.5, 4 and 6 week schedules are being developed; each should lead to useful improvements in local control but it is not yet known which schedule will be most effective.

Abnormal Matrix Remodeling in Adolescents and Young Adults with Kawasaki Disease Late after Onset

Patients with a history of Kawasaki disease (KD), have been found to have pericoronary and myocardial fibrosis. Serum biomarkers of fibrosis may be sensitive indices for detection of these late cardiac complications in KD patients. We studied a cohort of 60 adolescents and young adults comprising 10 KD patients with persistent coronary artery lesions (CAL) occurring at a mean (SD) time of 14.5 (4.4) years after disease onset, 25 KD patients with no CAL after disease onset, and 25 healthy age-matched volunteers. We compared laboratory data from the patients and volunteers, including lipid profile, liver function, amino-terminal propeptide of type III procollagen (PIIINP), matrix metalloproteinase 9 (MMP-9), tissue inhibitor of metalloproteinase 1 (TIMP-1), and MMP-9:TIMP-1 ratios. Severity of CAL was determined on the basis of computed tomography determinations of the frequency of aneurysms and the extent of coronary stenosis/occlusion, thrombosis, and calcification. Increased PIIINP and decreased MMP-9 and TIMP-1 concentrations and decreased MMP-9:TIMP-1 ratios were found not only in KD patients with persistent CAL but also in KD patients without CAL, although to a lesser extent in the latter group. In KD patients, the concentrations of PIIINP were positively associated with the severity of coronary stenosis/occlusion (r = 0.72, P = 0.011) and with the extent of coronary thrombus (r = 0.64, P = 0.014). The concentrations of high-sensitivity C-reactive protein, however, did not differ across groups. Our results demonstrate alterations in extracellular matrix biomarkers in KD patients, suggesting enhanced collagen synthesis and ameliorated degradation in adolescents and young adults late after the onset of KD. We also observed an association between the concentrations of PIIINP and the extent of coronary stenosis/occlusion or thrombosis in KD patients, a finding that needs confirmation in further studies.

Late Effects of Breast Radiotherapy in Young Women

Radiotherapy (RT) to the breast or chest wall of young women is associated with long-term cardiotoxicity and an increased risk of secondary breast cancers. As many patients with early stage breast cancer and Hodgkin's disease are cured of their disease, there is significant concern regarding the long term risks of therapy. Older RT techniques for treating the breast/chest wall and draining lymph nodes for breast cancer resulted in a relatively high dose being delivered to a substantial volume of heart, and convincing evidence exists of excess cardiovascular morbidity and mortality in patients treated with these techniques. While modern RT techniques have reduced radiation exposure to the heart, they have not eliminated it. Many large studies of Hodgkin's disease survivors have demonstrated a clear risk of secondary breast cancer development after mantle RT for Hodgkin's disease. The risk of developing breast cancer after mantle RT appears to be related to age at time of irradiation, dose delivered to the breast tissue, and whether or not chemotherapy is incorporated into the overall treatment plan. In this article we review late cardiac complications associated with tangential breast RT and the risk of developing a secondary breast cancer after mantle RT for Hodgkin's disease.

Early increases in cardiac troponin levels after major vascular surgery is associated with an increased frequency of delayed cardiac complications

Objective To evaluate changes in cardiac troponin–I levels after major vascular surgery and their association with early and late postoperative cardiac complications. Design Prospective, observational investigation. Setting University teaching hospital. Patients 75 consecutive patients undergoing major vascular surgery. Interventions All patients received a standard sevoflurane-fentanyl anesthesia during the procedure. Blood levels of creatine kinase with MB subtype and cardiac troponin–I were assessed before surgery and then everyday for the first 3 days after surgery. At the same time, 12-lead electrocardiography was also performed, and occurrence of any cardiac adverse event was recorded. Patients were then followed up for 1 month after surgery. Measurement and Main Results Troponin-I levels increased in 25 patients (33%) during the first 3 days after surgery; 9 of these patients (12%) had myocardial infarction. At univariate analysis, uncontrolled hypertension was the only risk factor for perioperative infarction (odds ratio, 16; (95% confidence interval, 3-74); however, multivariate logistic regression analysis failed to show statistically significant associations. Increases in troponin-I had a 100% sensitivity and 75% specificity in detecting myocardial ischemia with a 36% positive and 100% negative predictive values. Severe cardiac complication 1 month after surgery was reported in 5 patients (6.6%). The increase of cardiac troponin-I levels during the first 3 postoperative days was associated with an increased frequency of major cardiac complication at 1-month follow-up ( P = 0.003), with a 100% sensitivity, 71% specificity, and 100% negative predictive value. Conclusions Myocardial infarction after major noncardiac vascular surgery occurs in up to 12% of cases. Perioperative monitoring of troponin-I plasma levels may help to identify patients at increased risk for cardiac morbidity not only early after surgery but also during the first postoperative month.

Late sequelae of penetrating cardiac injuries

Fifty-four patients who survived a penetrating cardiac injury were assessed for late cardiac complications. The mean follow-up after injury was 23 months. Clinical history and physical examination suggested cardiac complications in nine patients (17 per cent). Electrocardiogram was abnormal, but usually not diagnostic, in 17 (31 per cent). Routine two dimensional Doppler echocardiography revealed abnormalities in 17 (31 per cent). Ten patients (19 per cent) had valvular or septal defects. Other abnormalities included pericardial effusion, ventricular and septal dysfunction, and ventricular dilatation. Although it is impossible to determine how many of these abnormalities were post-traumatic, it seems that the incidence of late sequelae of cardiac injuries is high, and it is recommended that routine late follow-up of these patients should be done. Assessment should include routine echocardiograms.

Cardiac troponin I assessment and late cardiac complications after carotid stenting or endarterectomy

When compared with carotid endarterectomy (CEA), percutaneous carotid angioplasty with stent replacement (CAS) is a less invasive technique in the treatment of carotid stenosis. However, periprocedural hemodynamic instability still remains a challenge. This instability might lead to myocardial damage, which is now measured accurately by using cardiac troponin I (CTnI). This study was designed to compare the periprocedural variation of CTnI in 150 consecutive patients scheduled to undergo CEA (n = 75) or CAS (n = 75). The levels of CTnI were measured until the third postoperative day in all patients. Short-term (1 month) and long-term (up to 5 years) postoperative cardiac outcome were assessed by means of chart review, regular follow-ups, and telephone calls. There was not any statistically significant difference between the 2 groups regarding the demographic characteristics and preprocedural medical status. The incidence of increase of CTnI (>0.5 ng/mL) was significantly higher in the CEA group (13%) compared with that in the CAS group (1%; P = .001). During the acute postprocedural period, the CAS group was significantly more prone to hypotension, requiring vasopressor therapy, whereas the CEA group had more hypertension, necessitating hypotensive medications (P < .001). At 5 years, the overall incidence of major cardiac complications (nonfatal myocardial infarction and death related to cardiac origin) was significantly more frequent in the CEA group (20% vs 5%, P < .01). The results of our study suggest that CAS yielded less myocardial damage in the short and long term when compared with CEA. Larger randomized multicenter trials with long-term outcomes are necessary to confirm our findings.

Cardiac complications of radiation therapy

To present an overview of cardiac complications arising from radiation therapy. Medline the (February 2004) and Embase (1974 to February 2004) searches of the medical literature relating to the cardiac complications of radiotherapy were conducted. Radiation damage may affect the pericardium, myocardium or coronary vasculature, and consists of fibrotic or small vessel damage. Cardiac complications are a particular problem with radiation treatments to the mediastinum and breast, especially when greater than 65% of the heart is irradiated. Most of the literature relates to the treatment of Hodgkin's disease, as patients with this disease tend to be young and live long enough to manifest late cardiac complications. Pericarditis, angina, myocardial infarction and arrhythmias are the most frequent causes of morbidity, with myocardial infarction being the most common fatal complication. The incidence of ischaemic heart disease does not increase rapidly until 10 years from treatment. Much of the evidence relates to the use of outdated radiation therapy equipment and techniques. Today's patients almost certainly have a lower risk of cardiac complications. Cardiac complications are probably under-reported, as they occur long after cured patients have been discharged from follow-up.