Development Of Myocardial Disease Research Articles

The Effect of Atenolol on CK-MB Levels in Hypertensive Patients

Atenolol is one of beta-adrenergic receptor blocking agent. It is widely used for the treatment of hypertension as a selective antihypertensive drug. But long term usage of atenolol may cause one of the cardiovascular diseases like myocardial infarction. To prove the relationship between atenolol and cardiovascular disease, measurement of creatinekinase-MB as a diagnostic indicator in early and long term usage of this drug by hypertensive patients is recommended. A comparative study was conducted in Al-Yarmouk Teaching Hospital–Emergency Department- on 30 hypertensive patients using atenolol. They were divided into (2) groups A and B according to the duration of the drug usage. Group A- (15) patients with a mean age (56+6) years. They used atenolol for a period of (1-5) years. Group B- also (15) patients with mean age (60+6) years. They used atenolol for (6-20) years. Both groups were with nearly the same number of males and females. All subjects of the study groups were screened to exclude evidence of hyper or hypothyroidism, diabetes and chronic renal failure. Venous blood samples were taken in first 8 hours after onset symptoms of cardiac attack from each patients and the levels of creatine kinase-MB were estimated and compared between the (2) groups. There is a significant correlation between levels of serum creatine kinase-MB of group A and group B (P<0.05). Atenolol causes increased level of serum CK-MB and this increase was directly proportional to the duration of the drug usage. CK-MB is one of cardiac markers that released from heart muscle when it is damaged as a result of myocardial infraction. So, atenolol has a significant correlation with development of myocardial diseases.
 Key words: hypertension , Atenolol and side effects , creatine kinase-MB , Atenolol antihypertensive.

Vascular diseases in CKD-MBD

Vascular calcification is an important component of CKD-MBD and occurs in association with vascular lesions of CKD-MBD such as atherosclerosis and arteriosclerosis. Atherosclerotic intimal calcification and medial calcification contribute to the development and progression of cardiovascular disease. Epidemiological data suggest that it is not atherothrombotic disease but myocardal disease including left ventricular hypertrophy with fibrosis and diastolic dysfunction which is the principal cause of cardiovascular death in CKD. Arteriosclerosis is characterized by thickening and calcification of the medial arterial layer. Medial calcification results in increased arterial stiffness and contributes to the development of myocardial disease. Therefore, it is important to develop novel therapeutics for medial calcification.

3,3′,5-triiodothyroxine inhibits apoptosis and oxidative stress by the PKM2/PKM1 ratio during oxygen-glucose deprivation/reperfusion AC16 and HCM-a cells: T3 inhibits apoptosis and oxidative stress by PKM2/PKM1 ratio

Oxidative stress (OS) plays a crucial role in the development of myocardial disease, which can induce the dysfunction of cardiac muscle cells. 3,3′,5-triiodothyroxine (T3) is a hormone secreted from the thyroid gland that has been shown to protect cells by improving the redox state and to regulate the expression of pyruvate kinase muscle isozyme (PKM, including two isoforms PKM1 and PKM2). The present study aimed to reveal the key effects of T3 on protecting human myocardial cell lines from oxidative stress and the downstream molecular mechanism. An oxygen-glucose deprivation/reperfusion model (OGDR) and three subtypes of the deiodinase family (DIO1, DIO2, and DIO3), which convert thyroxine (T4) to T3, were tested in this model. Our results show that the expression of DIO1, DIO2 and T3 was downregulated, but DIO3 was upregulated in OGDR-treated AC16 and HCM-a cells. Then, OGDR-treated cells were treated with T3 and T4. The results show that T3 inhibited the expression of reactive oxygen species (ROS) and malonic dialdehyde (MDA), but upregulated glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The effects of T4 were not notable. T3 also protected OGDR cells from apoptosis and upregulated the PKM2/PKM1 ratio. Further mechanistic studies found that PKM2 inhibition by small interfering RNA (siRNA) could attenuate the anti-OS and anti-apoptotic effects of T3. These findings suggest that T3 can inhibit apoptosis and oxidative stress in OGDR-treated AC16 and HCM-a cells by regulating the PKM2/PKM1 ratio.

Pharmacodynamic interaction of green tea extract with hydrochlorothiazide against ischemia-reperfusion injury-induced myocardial infarction.

Globally, the rate of development of myocardial diseases and hypertension is very common, which is responsible for incremental morbidity and mortality statistics. Treatment of ischemic hypertensive patients with diuretics such as hydrochlorothiazide (HCTZ) can precipitate myocardial infarction due to hypokalemia. This study was undertaken to evaluate the pharmacodynamic interaction of green tea extract (GTE) with HCTZ against ischemia-reperfusion induced myocardial toxicity. Wistar albino rats of either sex were taken and pretreated with high (500 mg/kg, p.o.) and low (100 mg/kg, p.o.) dose of GTE for 30 days. Standard, high and low dose of interactive groups received HCTZ (10 mg/kg, p.o.) for last 7 days. Ischemia-reperfusion injury was induced by modified Lagendorff apparatus, and the effect of different treatments was evaluated by percentage recovery in terms of heart rate and developed tension, serum biomarkers, and heart tissue antioxidant levels. Prophylactic treatment groups, such as high and low dose of GTE and their interactive groups with HCTZ, exhibited significant percentage recovery in terms of heart rate and developed tension. Apart from that, significant increase in superoxide dismutase and catalase, decrease in thiobarbituric acid reactive species in heart tissue, as well as significant decrease in serum lactate dehydrogenase, creatinine phosphokinase-MB and N-acetylcysteine levels have also been documented. The present findings clearly suggest that GTE dose-dependently reduces myocardial toxicity due to ischemia, and combination with HCTZ can reduce the associated side-effects and exhibits myocardial protection.

Tumor necrosis factor in myocardial hypertrophy and ischaemia--an anti-apoptotic perspective.

Time for primary review 21 days. Tumour necrosis factor-alpha (TNFα) is a multifunctional cytokine that has been implicated as mediator of diverse physiologic and pathophysiologic events. These processes include inflammation, cellular survival, growth, differentiation and apoptosis. The local homeostatic cellular effects of cytokines may be considered ‘autocoid’ in nature. This word is derived from the Greek words autos (‘self’) and akos (‘remedy’), and refers to locally acting, biologically active agents, both peptides and non-peptides, that are distinct from neurotransmitters and hormones [1]. Recent studies have highlighted the pathogenic role of TNFα in the development of myocardial disease, such as the direct correlation between serum TNFα levels and the severity and progression of heart failure [2–4] and the development of myocarditis in mice that overexpress TNFα specifically in the heart [5]. Taken together, these studies suggest that TNFα is a mediator of cardiac pathology, acting at least in part via inflammatory pathways and via the activation of programmed cell death i.e. apoptosis [6,7]. However, in addition to mediating inflammation and apoptosis, cytokines play a critical role in the control and maintenance of signalling pathways that regulate mammalian physiology in multiple organ systems. Specifically in the heart, biomechanical stress promotes endogenous TNFα production by myocytes and non-myocytes. Therefore, as in other organ systems, the question arising is whether TNFα plays an adaptive role in mediating cardiac cell growth and in remodelling the cardiac extracellular matrix in response to biomechanical stress. The hypothesis that TNFα could have a short term adaptive and long term maladaptive role was proposed and reviewed by Mann [8] in 1996. Recent studies support the view that TNFα can have beneficial effects in cardiac homeostasis. In this mini-review we will focus on the role of TNFα in mediating myocardial cell survival, growth and differentiation as adaptation … * Corresponding author. Tel.: +27-21-406-6358; fax: +27-21-447-8789 sack{at}samiot.uct.ac.za

Percutaneous transluminal coronary angioplasty and its role in thrombolysis: an overview of current practice

Percutaneous transluminal coronary angioplasty (PTCA) is now widely applied to sufferers of ischaemic heart disease who several years ago would have been referred for surgery, with success rates increasing as operator experience improves. Incurred hospital stay can be reduced from 10 days for surgery to 2 to 3 days for PTCA. Nursing care of these patients demands high standards of psychological care and potentially care of the critically ill. Nurses need to ensure their learning and research keeps up with the ever changing aspects of ischaemic heart disease. Since the GISSI study (Rovelli et al, 1986) was published thrombolytic therapy is now standard treatment for those suffering acute myocardial infarction (MI) within 6 hours of pain onset. New studies by ISIS-2 (1988) may even radically change the perceptions of time limits in these patients. After thrombolysis, a high grade lesion is often present to cause continuing pain or threat of re-closure. PTCA in these patients can relieve the patient equally as well at 10 days post-infarct as at immediate intervention, if the patient is clinically stable. Good post-therapy counselling services are essential in the long-term treatment of these sufferers to help reduce risk factors and therefore further development of myocardial disease.

Progress of research in cardiomyopathy and myocarditis in the USA

Research in cardiomyopathy and myocarditis is currently proceeding along several lines in the United States. Cardiomyopathy is becoming much better recognized on a clinical basis, and the various forms of myocardial disease are probably much more common than was ever before realized. Likewise, a great deal of interest has been kindled in the topic of myocarditis. A relative clarification of nomenclature and gradual adoption of the international terminology and classification of the cardiomyopathies is also occurring in the USA. Research into the possible etiologies of cardiomyopathies is most intense in the theory of infectious-immune causation of dilated cardiomyopathy. But also of great interest are studies into the role of vasculopathy, toxins, and the autonomic nervous system in the development of myocardial disease. Investigations into the infectious-immune theory involve both animal and human studies. Animal studies include viral infections with different strains to try and obtain a more suitable model for the human disease. Basic research in animals has also advanced our understanding of immunologic mechanisms of tissue injury in postinfectious phases, including the discovery of possible myocardial neoantigens eliciting an immune response. Human research continues in immunologic reactions in dilated cardiomyopathy patients, genetic makeup, and familial predispostions. Suppressor and natural killer cell function both appear abnormal in dilated cardiomyopathy patients. Endomyocardial biopsy is perhaps now more used and accepted than ever. Its use in research is pivotal from the standpoint of the elucidation of possible progression from myocarditis to cardiomyopathy, the biochemical and enzymatic constitution of diseased myocardium, beta receptor density, and immunologic reactions.

Dose-effect and structure-function relationships in doxorubicin cardiomyopathy

The cardiomyopathy (CM) produced by the anticancer drug doxorubicin (DXR) (Adriamycin) provides a unique opportunity to analyze dose-effect and structure-function relationships during development of myocardial disease. We measured the degree of morphologic damage by ultrastructural examination of endomyocardial biopsy and the degree of performance abnormality by right heart catheterization in patients receiving DXR. Morphologic damage was variable but was proportional to the total cumulative DXR dose between 100 and 600 mg/m 2. Performance abnormallties correlated weakly with dose, exhibited a curvillnear relationship, and had a “threshold” for expression. Catheterization abnormalitles correlated well with morphologic damage ( r = 0.57 to 0.78) in a subgroup of patients in whom exercise hemodynamics were measured, and this relationship also exhibited a curvilinear, threshold configuration. In DXR-CM myocardial damage is proportional to the degree of cytotoxic insult (DXR dose) while myocardial function is preserved until a critical dose or degree of damage is reached, after which myocardial performance deteriorates rapidly.