Cardiovascular Diseases & Diagnosis

Objective: To determine the relationship of serum troponin I after first acute myocardial infarction with left ventricular ejection fraction as assessed by echocardiography.

Methods: A total of 40 patients of acute myocardial infarction were included in the study. Troponin I concentration was measured by ELISA method and echocardiographic ejection fraction was calculated by modified Simpson’s rule. Echocardiographic ejection fraction was compared with serum troponin I concentration. Patients with previous myocardial infarction were excluded.

Result: There was strong negative correlation between troponin I concentration and left ventricular ejection fraction, i.e., with an increasing troponin level, there was a fall in ejection fraction. The Pearson’s correlation coefficient was –0.69, which was statistically significant (p<0.0001). In our study, we observed that patients with ejection fraction >50%, though small in number were having cTnI levels at 24 hrs ≤ 8 ng/ml. Patients with ejection fraction <50% (left ventricular systolic dysfunction) were having cTnI levels at 24 hrs ≥ 17 ng/ml. Therefore a presumptive cut off level of cTnI ≤ 8 ng/ml may be taken to consider normal left ventricular systolic function in STEMI. The normal range of Troponin I in apparently health individual without STEMI was observed to be <1.0 ng/ml. The mild increase in Troponin I at 24 hrs of STEMI with preserved EF >50% may be due to peak value of biomarker achieved at 24-36 hrs after myocardial injury as most of troponin I are attached to myofibrils.

Conclusion: Serum troponin I concentration has a strong negative correlation with left ventricular ejection fraction after first acute myocardial infarction, and hence can be used to assess the LVEF in patients with first myocardial infarction. An observation was made that a cut off level of cTnI ≤ 8 ng/ml was associated with normal left ventricular systolic function.

Background: The use of calcineurin inhibitors revolutionized transplantation by prolonging patients’ survival. However, their utility is limited by the development of significant chronic kidney disease.

Methods: We reviewed the English literature looking for recent publications regarding the management of chronic kidney disease in cardiac transplant patients. We chose relevant papers based on design, number of patients and clinical utility.

Results: Most publications on the subject involve small populations with few prospective, randomized studies. Early use of tacrolimus appears to be associated with better kidney function after one year compared to cyclosporine. Once chronic kidney disease is established, successful strategies include reduction or elimination of calcineurin inhibitors while relying on mycophenolate mofetil, proliferation signal inhibitors or anti-CD 25 antibodies to prevent rejection. There is no follow up longer than two years with these approaches. Kidney transplantation might offer improved long-term survival compared to dialysis in end-stage disease.

Conclusions: Prospective studies with long-term follow-up are needed to decide about the timing and to confirm the utility of replacing calcineurin inhibitors with other agents in cardiac transplant patients with chronic kidney disease.

Background: Myeloperoxidase (MPO), a heme peroxidase enzyme produced by macrophages, is a marker of oxidative stress associated with increased cardiovascular events in Diabetes Mellitus (DM). In this study we hypothesize that MPO protein and gene expression is associated with increased Intra-Plaque Hemorrhage (IPH), iron deposition, plaque inflammation and neovascularization in DM atheroma.

Methods: Twenty-six human aortas with advanced plaques (14 DM vs.12 No-DM) were studied. MPO protein and gene expression were quantified with immunohistochemistry and RT-PCR respectively. IPH was evaluated using H&E stain. Plaque iron was scored using Perl’s stain and graded Inflammatory cells and neovessels were manually counted in parallel sections using with (CD68 and CD3), and (CD34) using immunohistochemistry method.

Results: Total plaque MPO protein expression density (973.13 ± 28.32 vs. 356.24 ± 26.95; p = 0.0001) and MPO gene expression (0.00267 ± 0.0007 vs. 0.00033 ± 0.0001; p = 0.0001), IPH percentage (57.1% vs. 16.7 %; p= 0.04), iron grade (0.79 ± 0.21 vs. 0.25 ± 0.13; p = 0.05), inflammatory cell grade (1.71 ± 0.10 vs. 1.17 ± 0.11; p = 0.001) and total neovessel content (48.96 ± 4.68 vs. 21.54 ± 2.27; p = 0.0001) were significantly increased in DM plaques when compared to no-DM.

Conclusion: Increased MPO protein and gene expression are associated with a parallel increase in IPH, iron grade, inflammation grade and neovessel content in DM. This suggests a possible role of MPO in enhancing the IPH, iron deposition; inflammation and neovascularization in high risk DM plaques may possibly due to oxidative stress.

This report presents a case of cardiac tamponade that developed after a patient who presented with a pleuritic chest pain 2 weeks after pacemaker implantation. The patient developed cardiac tamponade after being treated with heparin drip for an incidental pulmonary embolism.

Neuregulin1s (NRG1s) are effective for protecting the heart from various stresses. Our previous studies show that heterozygous knockout of the NRG1 gene worsens while injections of a recombinant NRG1 improve cardiac function in Chemotherapy Drug Doxorubicin (DOX) - treated mice. In cultured cardiomyocytes, studies show that the Phosphoinositide 3-Kinase (PI3K) pathway is necessary for NRG1 to reduce DOX-induced apoptosis and loss of cardiac troponins. Here, we test whether PI3Kp110α, a Class IA PI3K isoform, is necessary for NRG1’s cardioprotective effects in DOX-treated mice. DOX was administered to mice with cardiomyocyte-specific overexpression of a constitutively active PI3Kp110α (CaPI3K), or a dominant negative PI3Kp110α (dnPI3K). Solvent or NRG1 was administered concurrently with DOX to dnPI3K mice. Our results showed that survival and cardiac function were improved in CaPI3K, but worsened in dnPI3K mice. Concurrent NRG1 injections significantly improved survival and cardiac function in dnPI3K mice, which were associated with increased activation of ERK1/2 and mTORC1 in the heart. These results have demonstrated that PI3Kp110α is important for protecting the heart from DOX. Further, the results suggest that PI3Kp110α is not necessary for NRG1 to protect the heart from DOX. NRG1 may protect the heart by activating alternative survival pathways, such as ERK1/2 and mTORC1, in DOX-treated dnPI3K mouse hearts.

We report a case of a large mobile right-sided heart thrombus (2.8 cm × 2.7 cm) complicated with pulmonary embolism. We planned to give thrombolytic therapy with an alteplase infusion and to repeat the TTE, and if the thrombus remained, to go ahead with surgical embolectomy with exploration of the right chambers and removal of the thrombus. Surgical removal of the thrombus with pulmonary embolectomy has been validated, but as it is a high-risk intervention, we were advised to try treatment with thrombolytic therapy first. Thrombolytic therapy resulted in complete disappearance of the thrombus, as documented by TTE. The patient was discharged home on oral anticoagulation with regular follow-up in outpatient clinic and lifelong anticoagulation was advised, as she was diagnosed to have type III protein S deficiency.

Resistin is derived mainly from fat tissue in rodents, and serum levels are elevated in animal models of obesity and insulin resistance. Recent clinical studies have demonstrated that circulating resistin is associated with inflammation, coronary atherosclerosis, renal dysfunction, adverse prognosis in patients with atherothrombotic ischemic stroke and heart failure. In the population-based observational study, increased circulating levels of resistin are associated with incidence of new-onset heart failure, even after accounting for prevalent coronary heart disease, obesity, insulin resistance, and inflammation. In the elderly, incident heart failure rates (per 1000 person-years) elevate with increasing baseline resistin concentrations. In addition, resistin is strongly associated with risk for incident heart failure in Cox proportional hazard models controlling for clinical variables, inflammatory biomarkers, and measures of adiposity.

The burden of advanced heart failure includes debilitating symptoms, frequent re-hospitalization and high rates of mortality. The most common causes of this preventable rehospitalization are patient’s failure to adhere to prescribed medicines and diet regimen. It is imperative that any medication counseling and educational program seeks to assess the patients understanding of their medical conditions and ability to appreciate the importance of medication compliance to their condition. A prospective cohort study involving 583 patients aged ≥ 30 years who met clinical criteria for presence of advanced heart failure on admission was done to assess the outcome of the program on mortality and re-hospitalization. 497 patients were discharge to the cardiac clinic for a 6-month follow up during which period they were taken through medication counseling and education on; Medication Compliance, Smoking, Alcohol, Diet and Nutrition, Salt restriction, Fluid intake, Weight loss and Exercise. The study showed 97.6% decrease in re-hospitalization rate and 12.4% decrease in mortality. Patients had also significantly improved in subjective and objective indices to functional status. 93.8% were classified within NYHA function class II and 6.2% in function class III. None of the patients remained in functional class IV as compared to 46.5% of the patients before discharge. The study showed that management of heart failure patients based on well structured medication education and counseling modalities can contribute to improved patients outcomes, including reduced morbidity and mortality rates, improved functional status and quality of life.