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The best-accepted definition of myocardial infarction (MI) is provided by statements from the Universal Definition of MI Global Task force. This article, now in its third iteration, defines MI as myocardial cell death due to prolonged myocardial ischemia. It further delineates an increasingly incident subclassification of MI known as type 2 MI (T2MI). T2MI identifies instances of myocardial necrosis in which an imbalance between myocardial oxygen supply and/or demand occurs for reasons other than atherosclerotic plaque disruption. While associated with considerable risk (comparable to that of type 1 MI, which has well-defined management strategies), the spectrum of potential etiologies for T2MI makes development of precise diagnostic criteria and therapeutic implications of the diagnosis challenging.

Magnesium is the fourth most abundant cation in the human body and is the second most prevalent cation in intracellular tissues. Myocardial cell action potentials are mediated by voltage-dependent Na+, K+, and Ca2+ channels which, when their function is altered, can lead to the genesis of cardiac dysrythmias. Magnesium regulates the movement of ions through these channels within myocardial tissues. The potential ability of magnesium supplementation to prevent and/or treat arrhythmias has been recognized in clinical medicine for years. This includes termination of torsade de pointes, prevention of post-operative atrial fibrillation, acute treatment of atrial fibrillation, and improving the efficacy and safety of antiarrhythmic drugs. Despite what is currently known about magnesium’s therapeutic potential, a number of limitations and gaps to the literature exist. This includes an unclear link between correction of intracellular magnesium concentrations and both mechanistic and clinical outcomes, small sample sizes, varying routes of administration and doses, as well as short follow-up periods. This review highlights these gaps and recommends areas of need for future research.

BACKGROUND: Cardiac troponins have emerged as the preferred biomarkers for detecting myocardial necrosis and diagnosing myocardial infarction. However, current cardiac troponin assays do not discriminate between ischemic and nonischemic causes of myocardial cell death. Thus, when an increased troponin value is encountered in the absence of obvious myocardial ischemia, a careful search for other clinical conditions is crucial.METHODS: In 2010 to 2011, we prospectively studied hospitalized patients who had cardiac troponin I measured on clinical indication. An acute myocardial infarction was diagnosed in cases of a cardiac troponin I increase or decrease pattern with at least 1 value >30 ng/L (99th percentile) together with myocardial ischemia. Myocardial injury was defined as cardiac troponin I values >30 ng/L, but without signs or symptoms indicating overt cardiac ischemia. Patients with peak values ≤30 ng/L were classified as nonelevated cardiac troponin I. Follow-up was at least 3 years with all-cause mortality as the sole clinical end point.RESULTS: A total of 3762 patients were included. Of these, 488 (13%) had acute myocardial infarction, 1089 (29%) had myocardial injury, and 2185 (58%) had nonelevated cardiac troponin I values. Patients with myocardial injury frequently presented with dyspnea, were older, and had more comorbidity than patients in the 2 other groups. During a median follow-up of 3.2 years, 1342 patients died. Mortality differed significantly between groups: 39% in those with myocardial infarction, 59% in those with myocardial injury, and 23% in those with nonelevated cardiac troponin I (log-rank test; P < .0001). No significant difference in mortality between patients with type 2 myocardial infarction and patients with myocardial injury was observed (63% and 59%, respectively).CONCLUSIONS: Patients with myocardial injury are older and have more comorbidity than those with acute myocardial infarction. Both groups exhibit a poorer prognosis than patients with nonelevated cardiac troponin I values. Of note, a very high long-term mortality is observed in patients with type 2 myocardial infarction and patients with myocardial injury.

The clinical use of doxorubicin is limited by the total cumulative dose due to its dose-related cardiac toxicities. Clinical manifestation of doxorubicin-mediated cardiotoxicity may be presented in forms of arrhythmia, cardiomyopathy, or congestive heart failure. Cardiomyopathy is a condition in which the cardiac muscles are damaged, leading to cardiac dysfunctions. Mechanistically, the damage of cardiomyocytes is believed to be mediated primarily by oxidative stress. Cardiac mitochondrial damage is evident within a few hours following exposure to doxorubicin. When cardiomyocytes are chronically exposed to doxorubicin, the damages are even more pronounced. In animal models of doxorubicin-induced cardiotoxicity, lacking multidrug-resistance associated protein 1 intensifies damage of the cardiac nuclei and causes more severe left ventricular dysfunction. It appears that cardiac tissue damage induced by doxorubicin is not confined to cardiomyocytes; endothelial cells are affected by doxorubicin as well. Current evidence has indicated that there is a cross-talk between endothelial cells and cardiomyocytes. The purpose of this article is to briefly review and update the current findings associated with doxorubicin-induced cardiomyopathy.

We exclusively analyze the onset and condition of formation of modulated waves in a diffusive FitzHugh–Nagumo model for myocardial cell excitations. The cells are connected through gap junction coupling. An additive magnetic flux variable is used to describe the effect of electromagnetic induction, while electromagnetic radiation is imposed on the magnetic flux variable as a periodic forcing. We used the discrete multiple scale expansion and obtained, from the model equations, a single differential-difference amplitude nonlinear equation. We performed the linear stability analysis of this equation and found that instability features are importantly influenced by the induced electromagnetic gain. We present the unstable and stable regions of modulational instability (MI). The resulting analytic predictions are confirmed by numerical experiments of the generic equations. The results reveal that due to MI, an initial steady state that consisted of a plane wave with low amplitude evolves into a modulated localized wave patterns, soliton-like in shape, with features of synchronization. Furthermore, the formation of periodic pulse train with breathing motion presents a disappearing pattern in the presence of electromagnetic radiation. This could provide guidance and better understanding of sudden heart failure exposed to heavily electromagnetic radiation.

Cardiac troponin I (TnI) is a cardiac specific regulatory protein that has been proven to be important in tracking myocardial cell injury and future mortality. Studies have proposed increases in TnI can often identify cardiovascular (CV) complications that correlate with increased mortality for non

As a specific intracellular enzyme of myocardial cells, cardiac Troponin I (CTnI) is detectable in trace amount in normal population blood. Any increase of CTnI is suggestive of myocardial cell injury. This study sought to examine the relation between CTnI and subclinical coronary artery disease (