Question

Which agent prevents myocardial cell calcium overload and thereby decreases ventricular wall tension? (A) ranolazine (B) nitroglycerin (C) amlodipine (D) ivabradine (E) trimetazidine

Short answer

The agent is (A) ranolazine.

Step-by-step solution

Identify the Mechanism of Each Agent

To solve this problem, we need to understand how each agent works. Ranolazine works by inhibiting the late sodium current, which reduces calcium overload in myocardial cells. Nitroglycerin primarily works by vasodilation, reducing preload and afterload. Amlodipine is a calcium channel blocker that primarily affects vascular smooth muscles. Ivabradine reduces heart rate by inhibiting the If current in the sinoatrial node. Trimetazidine preserves myocardial energy metabolism during ischemia.

Determine the Effect on Calcium Overload

The direct effect on calcium overload in myocardial cells is primarily a characteristic of ranolazine. By inhibiting the late sodium current, ranolazine indirectly reduces calcium influx into the cell, which alleviates calcium overload and decreases ventricular wall tension.

Select the Correct Answer

Given that only ranolazine directly affects intracellular calcium overload by inhibiting the late sodium current, it is the agent that prevents myocardial cell calcium overload and decreases ventricular wall tension. Therefore, the correct answer is (A) ranolazine.

Key concepts

Myocardial Cell Calcium Overload

Myocardial cell calcium overload occurs when there is an excessive accumulation of calcium ions within the heart muscle cells. This imbalance can lead to several cardiac problems, as calcium plays a key role in muscle contraction. When muscle cells are overloaded with calcium, they contract more forcefully, and this can cause increased strain on the heart.

Causes of calcium overload often include dysfunction in the movement of ions across the cell membrane, particularly through the sodium and calcium exchange processes. Effective management of this condition is crucial, as it helps prevent the progression of further cardiac issues.

• Excessive calcium leads to dysregulated heart contractions.
• Can result in arrhythmias or heart failure if left untreated.

Understanding how medications can modulate calcium levels in myocardial cells is critical in cardiac pharmacology.

Ventricular Wall Tension

Ventricular wall tension is the force exerted by heart muscle as it contracts. High tension can lead to the thickening of the heart muscle, a condition known as hypertrophy. This condition often results in increased pressure during heartbeats, making it heart work harder.

The tension in the ventricular walls is a product of several factors, including blood pressure and the volume of blood in the heart during the contraction. Managing ventricular wall tension is important because prolonged high tension can weaken the heart over time.

• Results in the heart working harder than normal.
• Can increase the risk of heart disease if not controlled.

Medications that can reduce calcium overload are often employed to reduce wall tension.

Ranolazine Mechanism

The mechanism of action of ranolazine involves inhibiting the late sodium current in myocardial cells. This specific action helps to prevent the calcium overload by minimizing intracellular sodium levels, which, in turn, reduces calcium influx.

Ranolazine is uniquely positioned to target the cascade of events leading to calcium overload, thereby decreasing ventricular wall tension. This effect is particularly beneficial in individuals suffering from ischemic heart conditions. By acting selectively, it ensures a protective role against myocardial stress.

• Inhibits the late sodium current.
• Reduces intracellular sodium and calcium overload.

This mechanism supports its use in managing conditions like angina, where excessive wall tension can exacerbate symptoms.

Pharmacological Agents Effects

Understanding the effects of pharmacological agents is key in selecting the right treatment for cardiac conditions. Different drugs work through various mechanisms to address heart-related issues.

Agents like nitroglycerin, amlodipine, and ivabradine each have distinct actions that do not specifically target calcium overload in myocardial cells, unlike ranolazine. While all are used in treating cardiac conditions, none effectively reduce calcium levels in the way ranolazine does.

• Nitroglycerin acts primarily as a vasodilator.
• Amlodipine is a calcium channel blocker that lowers blood pressure but doesn’t address calcium overload.
• Ivabradine primarily reduces heart rate.

Each pharmacological agent has unique applications, with ranolazine’s specific action against calcium overload offering a valuable approach to reducing myocardial stress.