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The traditional Chinese medicine prescription "Sheng-Mai-San (SMS)" has been used for treating patients with coronary heart disease for a long time and was found to have antioxidative effects. Here, we applied adriamycin (doxorubicin, ADR), a highly effective anticancer agent, as an inducer to establish the animal model of dose-related cardiomyopathy due to inhibition of nucleic acid as well as protein synthesis, formation of free radicals, and lipid peroxidation. The objective of this study was to investigate the protective effects of SMS on adriamycin-induced cardiomyopathy. Wistar rats were divided into four groups: CONT (control), ADR, SMS, and ADR + SMS. ADR (cumulative dose, 15 mg/kg) was administered to rats in six equal intraperitoneal injections over a period of 2 weeks and SMS was administered via a feeding tube throughout the mouth once a day for 30 days (cumulative dose, 150 g/kg). At the end of the 5-week post-treatment period, the hearts of the rats were surgically removed for the study of synthesis rates of DNA, RNA and proteins. Besides myocardial antioxidants, lipid peroxidation and morphological ultrastructure were also evaluated. Three weeks after the treatment, cardiomyopathy and congestive heart failure were characterized according to assessment in ascites, congested liver, depressed cardiac function and myocardial cell damage. The results demonstrated that nucleic acid as well as protein synthesis was inhibited, while lipid peroxidation was increased. Myocardial glutathione peroxidase (GSHPx) activity was decreased and electron microscopic examination revealed myocardial lesion indicative of ADR-induced cardiomyopathy. In contrast, administration of SMS before and concurrent with ADR significantly attenuated the myocardial effects. It also lowered mortality as well as the amount of ascites. In addition, indexes in myocardial GSHPx, macromolecular biosynthesis and superoxide dismutase activities were increasing, with a concomitant decrease in lipid peroxidation and preserved myocardial ultrastructure. These results indicated that SMS may be partially protective against ADR-induced cardiomyopathy.

Phytochemical flavonoids have been proven to be effective in treating various disorders, including cardiovascular diseases. Acacetin is a natural flavone with diverse pharmacological effects, uniquely including atrial-selective anti-atrial fibrillation (AF) via the inhibition of the atrial specific potassium channel currents $I_{\mathrm{\text{Kur}}}$ (ultra-rapidly delayed rectifier potassium current), $I_{\mathrm{\text{KACh}}}$ (acetylcholine-activated potassium current), $I_{\mathrm{\text{sKCa}}}$ (calcium-activated small conductance potassium current), and $I_{\mathrm{\text{to}}}$ (transient outward potassium current). $I_{\mathrm{\text{to}}}$ inhibition by acacetin, notably, suppresses experimental J-wave syndromes. In addition, acacetin provides extensive cardiovascular protection against ischemia/reperfusion injury, cardiomyopathies/heart failure, autoimmune myocarditis, pulmonary artery hypertension, vascular remodeling, and atherosclerosis by restoring the downregulated intracellular signaling pathway of Sirt1/AMPK/PGC-1α followed by increasing Nrf2/HO-1/SOD thereby inhibiting oxidation, inflammation, and apoptosis. This review provides an integrated insight into the capabilities of acacetin as a drug candidate for treating cardiovascular diseases, especially atrial fibrillation and cardiomyopathies/heart failure.

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A three-year-old neutered male mixed-breed cat was referred for tachypnea, decreased appetite, and lethargy due to a pleural effusion secondary to myocardial failure. Severe left atrial (LA) and left ventricular (LV) dilation, extremely decreased fractional shortening of the LV, and spontaneous echocardiographic contrast in the LA appendage were noted on an echocardiogram. Medical treatments included furosemide, pimobendan, benazepril, clopidogrel, and taurine supplementation. During follow-up visits, tachypnea was not observed, and his activities and appetite returned to normal. Echocardiography showed normal LA and LV chambers and increased LV fractional shortening. The point-of-care test result for N-terminal pro-brain natriuretic peptide (NT-proBNP) was abnormal during the first two visits (day 1 and day 16), and the concentration of plasma NT-proBNP was 1500pmol/L and 349pmol/L, respectively. On the third and fourth visits (day 35 and day 70), the point-of-care test result for NT-proBNP was normal and corresponded with normal echocardiography findings.

Background: Recently biventricular pacing showed to be a good treatment option to patients with congestive heart failure and important ventricular dysfunction with wide QRS complex. However a few patients do not respond with a clinical improvement. Objective: Identify the patients that are benefited of this boarding using the 87-lead Body Surface Potential Mapping (BSPM). Methods and Results: Twenty seven patients with dilated cardiomyopathy and biventricular pacing were studied. All of them were submitted to BSPM, that measure total and regional (right ventricle, septum and left ventricle) ventricular activation times (VAT) before and after biventricular pacing implantation. After biventricular pacing implantation, all of the 27 patients presented with a narrower QRS complex using simultaneous 12-lead ECG from BSPM (179±19ms × 159±21ms, p=0.001), and 2 groups were identified: GI, with increased ejection fraction (37%±9%) and GII, with worse ejection fraction (23%±70%). Total and regional ventricular activation time of both groups were then compared. Group II showed a significant increase in total ventricular activation time when compared to the basal situation (179±27ms × 221±38ms, p=0.01), exclusively due to right ventricle activation prolongation (47±15ms × 86±18ms, p<0.0001). Although group I also presented an increase of total VAT, it was not significant (169±37ms × 182±95ms, p=ns). Conclusion: Body Surface Potential Mapping is an useful tool to identify the patients that will be benefited from biventricular pacing using total and regional ventricular activation time.

Cardiomyopathy, a condition in which the heart muscle does not work properly, can affect children and adults. Unlike heart disease due to heart attack, where there is a problem with adequate blood flow to the heart, cardiomyopathy refers to the disease of heart muscle itself. The common types of cardiomyopathy are dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and specific cardiomyopathy. The causes of cardiomyopathy are unknown, and these diseases can be inherited or caused by other diseases or environmental toxicants. Coronary artery disease causes ischemic cardiomyopathy. Alcohol, especially when a person has a poor diet, causes alcoholic cardiomyopathy. Toxicants, including the anticancer drug doxorubicin, cause toxic cardiomyopathy. Chronic diseases such as diabetes cause disease-related cardiomyopathy, for instance, diabetic cardiomyopathy. Although there are distinct mechanisms for these cardiomyopathies with different etiologies, there are also certain common pathogenic mechanisms; exploring these common mechanisms will be of great importance for developing preventive approaches to these cardiomyopathies. Metallothionein as a stress protein (adaptive protein) was found to play a critical role in protecting the heart from a variety of pathogenic and environmental risks. Therefore, this chapter will summarize the protective effects of metallothionein on the development of these cardiomyopathies, focusing on the experimental evidence, possible mechanisms, and potential clinical implications.