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Heart Failure Drugs: Inotropic Agents01:26

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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...
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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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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,...
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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Heart Failure III: Clinical Manifestations01:26

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Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
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Fingolimod effects on left ventricular function in multiple sclerosis.

Vittorio Racca1, Marco Di Rienzo2, Rosella Cavarretta3

  • 1Cardiology Rehabilitation Department, Santa Maria Nascente Institute IRCCS, Don Carlo Gnocchi Foundation, Italy vracca@dongnocchi.it.

Multiple Sclerosis (Houndmills, Basingstoke, England)
|June 5, 2015
PubMed
Summary
This summary is machine-generated.

Fingolimod treatment in multiple sclerosis (MS) patients can reduce left ventricular systolic function, indicated by decreased ejection fraction. Caution is advised for patients with pre-existing heart conditions.

Keywords:
Fingolimodcardiotoxicitydrug safetydrug side effectsleft ventricular systolic functionmultiple sclerosisventricular ejection fraction

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Area of Science:

  • Cardiology
  • Neurology
  • Pharmacology

Background:

  • Cardiovascular side effects like bradycardia and atrioventricular block were noted in early fingolimod trials for multiple sclerosis (MS).
  • A post-marketing cardiovascular-related death has been reported, highlighting concerns about fingolimod's cardiac safety.

Purpose of the Study:

  • To evaluate the medium-term impact of fingolimod on heart function.
  • To gain deeper insights into the cardiac safety profile of fingolimod in MS patients.

Main Methods:

  • Echocardiography assessed cardiac function in 53 patients on fingolimod (0.5 mg daily) and 25 on natalizumab (300 mg monthly).
  • Assessments were conducted at baseline (T0), 1 month (T1), 6 months (T6), and 12 months (T12) for the fingolimod group.

Main Results:

  • Fingolimod significantly decreased mean left ventricular ejection fraction and increased end-systolic volume from T0 to T1 and T6 (p<0.0001).
  • These cardiac function changes were not observed in the natalizumab group, though a slight increase in ejection fraction was seen at T12.
  • Nine patients switched from natalizumab to fingolimod also showed a similar decrease in ejection fraction after six months.

Conclusions:

  • Fingolimod significantly impairs left ventricular systolic function in multiple sclerosis patients.
  • While generally without clinical consequence in patients without prior cardiac issues, the findings necessitate increased caution in those with current or past heart failure.