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Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...

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Crystal structure of the (1<i>R</i>,2<i>S</i>,5<i>R</i>) diastereomer of acoltremon, C<sub>18</sub>H<sub>27</sub>NO<sub>2</sub>, from synchrotron powder diffraction data and density functional theory calculations.

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Updated: Jun 9, 2026

Transcatheter Pulmonary Valve Replacement from Autologous Pericardium with a Self-Expandable Nitinol Stent in an Adult Sheep Model
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Published on: June 8, 2022

Levosimendan Form I, C14H12N6O.

Jacob K Salazar1, James A Kaduk2, Anja Dosen3

  • 1North Central College, Department of Chemistry 131 S Loomis St Naperville IL 60540 USA.

Acta Crystallographica. Section E, Crystallographic Communications
|June 8, 2026
PubMed
Summary
This summary is machine-generated.

The crystal structure of levosimendan Form I was solved using X-ray powder diffraction and density functional theory. This reveals its P212121 space group and layered molecular stacking stabilized by hydrogen bonds.

Keywords:
Rietveld refinementSimdax®density functional theorylevosimendanpowder diffraction

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Published on: September 24, 2021

Area of Science:

  • Crystallography
  • Materials Science
  • Computational Chemistry

Background:

  • Levosimendan is a calcium sensitizer used in treating acute decompensated heart failure.
  • Understanding the solid-state structure of drug compounds is crucial for formulation and bioavailability.
  • Polymorphism in drug substances can significantly impact their physicochemical properties.

Purpose of the Study:

  • To determine the crystal structure of levosimendan Form I.
  • To elucidate the intermolecular interactions and packing in levosimendan Form I.
  • To provide a structural basis for understanding levosimendan's solid-state behavior.

Main Methods:

  • Synchrotron X-ray powder diffraction (XRPD) for crystal structure determination.
  • Density Functional Theory (DFT) for structural optimization.
  • Analysis of hydrogen bonding and molecular packing.

Main Results:

  • The crystal structure of levosimendan Form I was solved and refined.
  • Levosimendan Form I crystallizes in the P212121 space group.
  • Molecules exhibit nearly parallel stacking along the bc plane, linked by N-H⋯O and N-H⋯N hydrogen bonds.

Conclusions:

  • The detailed crystal structure of levosimendan Form I has been established.
  • The identified hydrogen bonding patterns dictate the layered crystal packing.
  • This structural information is vital for future pharmaceutical development and polymorph control of levosimendan.