Nutrient Deficiency and Drug Induced Cardiac Injury and Dysfunction

Cardiac injury manifested as either systolic or diastolic dysfunction is considered an important preceding stage leading to or associated with eventual heart failure. There is increasing literature recognizing that deficiency and/or imbalance of certain essential micronutrients, vitamins, and macrominerals may be involved in the pathogenesis of cardiomyopathy/injury/contractile dysfunction. Essential micronutrients may include, but not limited to, water soluble B vitamins such as thiamine, vitamin C, fat-soluble vitamins (A, E, D, K), carnitine, Coenzyme Q10, and taurine (a conditionally essential amino acid), as well as microminerals, such as selenium, zinc, copper, cobalt, and chromium. Notable macrominerals may include magnesium, calcium, iron, and potassium. While much of the nutritional deficiency might be caused by poor dietary intake, certain nutrient deficiencies, especially of Mg leading to hypomagnesemia, may be caused by excessive alcohol intake, antiretroviral drug treatments of HIV/AIDS patients, or anticancer therapeutics such as epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) and cisplatin. Anticancer drugs may cause kidney injury and dysfunction, leading to malabsorption of Mg and renal Mg wasting. Many of the listed micronutrients are co-factors of metabolic reactions, and their deficiency would disturb myocardial substrate metabolism and energy utilization. Mg plays a key role in modulating neuronal excitation, endothelial function, and cardiac contraction by regulating several ion channels, including K and Ca; Mg is also a key co-factor for mitochondrial ATP production. As such, Mg deficiency may contribute to the pathogenesis of cardiac arrhythmias and dysfunction. Iron can be a pro-oxidant mineral, but iron is essential for the development of normal red blood cells and healthy immune function, and its deficiency is the most widespread nutritional deficiency in the world.

While it remains unclear if any chronic nutrient deficiency-induced cardiac injury/dysfunction is readily reversible, no consistent nutritional supplementation has been recommended as a rescue strategy against cardiac injury/dysfunction. It is noted that many of the micronutrients have antioxidant properties (e.g., vitamins E and C, selenium, and Coenzyme Q10). Mg is a natural calcium blocker, and its elevated intake above normal levels may also produce antioxidative, anti-inflammatory effects in vivo. The purpose of this Special Issue is to provide a platform for recent experimental or clinical research that may shed new light on nutrient/mineral deficiencies or adverse drug effects that may impair cardiac function directly or indirectly. Common mechanistic parameters may involve systemic oxidative/nitrosative stress, neurogenic inflammation, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, oxidative/antioxidant gene up-regulation, and/or compromised antioxidant defenses, which may serve as prognostic mediators/events linked to induced cardiac injury/dysfunction. The ultimate goal is to search for a better understanding of the complex interactions and molecular mechanisms contributing to cardiac injury/dysfunction and potential effective mitigating interventions.

Prof. Dr. I.Tong Mak
Prof. Dr. Jay H. Kramer
Guest Editors

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• Cardiac injury/contractile dysfunction
• Micronutrient deficiency
• Macromineral deficiency or imbalance
• Impact by cardiovascular and/or anti-cancer drugs
• Systemic inflammation
• Oxidative/nitrosative stress
• Antioxidant defenses
• Supplement and/or pathway interventions