Thank you for visiting congestive heart failure symptom website.
Let me briefly introduce myself. My name is Sergey. I am 44 years old. In
a fall of 2005 I was diagnosed with congestive heart failure symptom. My
strong believe that it happened because I was on tryciclic antidepressant
nortriptyline (100mg. Daily) for 2 years.
This site is my attempt to put together my research about adverse effects
of nortriptyline in general, heart-damaging effects in particular. If you have
unfortunate experience dealing with nortriptyline and would like to share
your knowledge with others please Email to email@example.com
Hank you once again for visiting congestive heart failure symptom website
Patients with cardiovascular disease should be given nortriptyline only
under close supervision because of the tendency of the drug to produce
sinus tachycardia and to prolong the conduction time. Both elevation and
lowering of blood sugar levels have been reported.
Adverse Effects. Note:
Included in the following list are a few adverse reactions that have not been
reported with this specific drug. However, the pharmacologic similarities
among the tricyclic antidepressant drugs require that each of these
reactions be considered when nortriptyline is administered.
Hypotension, hypertension, tachycardia, palpitation, myocardial infarction,
arrhythmias, heart block, stroke, congestive heart failure symptom.
Overdose of tricyclic antidepressants may be manifest with doses as small
as 50 mg in a child. Of patients who are alive at initial presentation, a
mortality rate of between 0% and 15% has been reported. Symptoms of
overdose of tricyclic antidepressants may begin within several hours of oral
ingestion. Symptoms and signs may include blurred vision, confusion,
restlessness, dizziness, hypothermia, hyperthermia, agitation, vomiting,
hyperactive reflexes, dilated pupils, fever, rapid heart rate, decreased
bowel sounds, dry mouth, inability to void, myoclonic jerks, seizures,
respiratory depression, myoglobinuric renal failure, nystagmus, ataxia,
dysarthria, choreoathetosis, coma, hypotension, and cardiac arrhythmias.
An effect on cardiac conduction similar to that of quinidine may be seen
with slowing of conduction, prolongation of the QRS complex and QT
intervals, right bundle branch and AV block, ventricular tachyarrhythmias
(including Torsade de pointes and fibrillation), and death. Prolongation of
the QRS duration to more than 0.1 seconds is predictive of more severe
toxicity. The absence of sinus tachycardia does not ensure a benign course.
Hypotension may be caused by vasodilation, central and peripheral alpha-
adrenergic blockade, and cardiac depression. In a healthy young person,
prolonged resuscitation may be effective; one patient was reported to
survive 5 hours of cardiac massage.
Tricyclic antidepressant poisoning : cardiovascular toxicity.
Thanacoody HK, Thomas SH.
Wolfson Unit of Clinical Pharmacology, School of Clinical and Laboratory
Sciences, University of Newcastle, and National Poisons Information Service
(Newcastle Centre), Newcastle upon Tyne, UK.
Tricyclic antidepressants remain a common cause of fatal drug poisoning as
a result of their cardiovascular toxicity manifested by ECG abnormalities,
arrhythmias and hypotension. Dosulepin and amitriptyline appear to be
particularly toxic in overdose. The principal mechanism of toxicity is cardiac
sodium channel blockade, which increases the duration of the cardiac action
potential and refractory period and delays atrioventricular conduction.
Electrocardiographic changes include prolongation of the PR, QRS and QT
intervals, nonspecific ST segment and T wave changes, atrioventricular
block, right axis deviation of the terminal 40 ms vector of the QRS complex
in the frontal plane (T 40 ms axis) and the Brugada pattern (downsloping
ST segment elevation in leads V1-V3 in association with right bundle branch
block). Maximal changes in the QRS duration and the T 40 ms axis are
usually present within 12 hours of ingestion but may take up to a week to
resolve. Sinus tachycardia is the most common arrhythmia due to
anticholinergic activity and inhibition of norepinephrine uptake by tricyclic
antidepressants but bradyarrhythmias (due to atrioventricular block) and
tachyarrhythmias (supraventricular and ventricular) may occur. Torsade de
pointes occurs uncommonly. Hypotension results from a combination of
reduced myocardial contractility and reduced systemic vascular resistance
due to alpha-adrenergic blockade. Life-threatening arrhythmias and death
due to tricyclic antidepressant poisoning usually occurs within 24 hours of
ingestion. Rapid deterioration is common. Level of consciousness at
presentation is the most sensitive clinical predictor of serious congestive
heart failure symptom. Although a QRS duration >100 ms and a rightward
T 40 ms axis appear to be better predictors of cardiovascular toxicity than
the plasma tricyclic drug concentration, they have at best moderate
sensitivity and specificity for predicting complications.
[Reversible cardiomyopathy induced by psychotropic drugs: case report and
literature overview] Ann Cardiol Angeiol (Paris). 2002; 51(6):386-90
(ISSN: 0003-3928) Cruchaudet B; Eicher JC; Sgro C; Wolf JE Centre de
cardiologie clinique et interventionnelle, hôpital du Bocage, CHU Dijon, 2,
boulevard Maréchal-de-Lattre-de-Tassigny, 21034 Dijon, France. jean-
firstname.lastname@example.org A number of psychotropic drugs, including
tricyclic antidepressants, phenothiazine and lithium, have a well
demonstrated risk of cardiotoxicity. Each individual therapeutic class has
potentially deleterious effects on electrophysiology and myocardial function.
The authors report a case showing how serious side effects may result from
the association of these different classes in the presence of a coexistent
heart disease, even when the underlying disease is mild. Psychotropic
medication and the heart Patrick O’Brien and Femi Oyebode http://apt.
rcpsych.org/cgi/content/full/9/6/414 The cardiotoxicity and mortality from
overdose of tricyclic antidepressants is well established. Toxicity arises from
sodium (Na+) ion-channel blockade, known as Type 1 antiarrhythmic
action. This reduces inward Na+ depolarising current at the beginning of the
action potential, leading to conduction delay, bradycardia, atrioventricular
block, bundle branch block and monomorphic ventricular tachycardia.
Toxicity, Tricyclic Antidepressant (TCA) Last Updated: August 2, 2004
Medical/Legal Pitfalls: Failure to recognize new onset of ventricular
arrhythmia as a direct consequence of TCA overdose
Toxicity, Antidepressant Last Updated: January 5, 2006 Frequency: ·
In the US: According to the Toxic Exposure Surveillance System (TESS) data
from the American Association of Poison Control Centers (AAPC), 12,710
cyclic antidepressant exposures were reported in 2003.
Amitriptyline accounted for most exposures with 7,309 (58%). Of all TCA
exposures, 7,835 (62%) were intentional overdoses, 9,622 (76%) were
treated at a health care facility, 1,373 (11%) resulted in major toxicity, and
93 (0.007%) resulted in death. In 1998, 15,710 cyclic antidepressant
exposures were reported in the United States; of these exposures, 1694
(11%) resulted in major toxicity and 88 (0.6%) resulted in fatality. Most
exposures were intentional and required treatment in a health care facility.
TCA use has declined in relation to the newer, less toxic, selective
serotonin reuptake inhibitor (SSRI) antidepressants, but TCAs remain
widely prescribed and are among the most commonly reported drugs
associated with overdose. TCAs are used for depression but also are
prescribed for nontraditional uses (eg, chronic pain syndromes, migraine
prophylaxis, peripheral neuropathies). http://www.freerepublic.
com/forum/a38fdc122664b.htm Boy apparently dies from longterm ritalin
use. As of 1993, there had been 4 sudden deaths associated with
Norpramin (desipramine), a member of the family of tricyclic
antidepressants (TCAs) and a common alternative to Ritalin, in the
treatment of ADHD. In 1995, Werry, of New Zealand, called for an embargo
of desipramine in children, but was shouted down by Biederman, et al, of
the Harvard-Massachusetts General Hospital, Pediatric Psychopharmacology
Group. To date, desipramine- and other TCA-related, sudden, cardiac
deaths have risen to 16, most of them in normal children said by school
teachers, to have ADHD.
Sudden cardiac death with clozapine and sertraline combination
JD Hoehns, MM Fouts, MW Kelly, and KB Tu
OBJECTIVE: To report a case of sudden cardiac death in a patient receiving
combination therapy with clozapine and sertraline. CASE SUMMARY: A 26-
year-old white man was discovered dead at his residence. His medical
history included chronic paranoid schizophrenia, obsessive-compulsive
disorder, major depressive disorder, obstructive sleep apnea, and
akathisia. He had no prior history of cardiovascular disease. His medication
regimen included clozapine 100 mg twice daily (started 4 y prior to his
death), risperidone 3 mg twice daily, sertraline 200 mg once daily, atenolol
50 mg twice daily, and lorazepam 0.5 mg four times daily. Autopsy and
toxicology studies revealed cardiomegaly suggestive of idiopathic
cardiomyopathy, single-vessel coronary artery disease, sertraline and
clozapine blood concentrations in the expected range, undetectable
lorazepam and risperidone blood concentrations, obesity, and moderate
fatty changes to the liver. The most likely cause of death was sudden
cardiac death due to acute cardiac arrhythmia. DISCUSSION: Clozapine is
structurally similar to the tricyclic antidepressants, which have type 1 A
antiarrhythmic properties. Case reports have described electrocardiographic
abnomalities, cardiomyopathy, and fatal myocarditis associated with its
use. Unexplained death in patients on clozapine therapy has also been
reported. Sertraline appears to have less cardiac effect; however, one
report has observed clinically significant QT prolongation during sertraline
therapy. CONCLUSIONS: Clozapine-induced cardiomyopathy and cardiac
arrhythmia from clozapine and/or sertraline use may have contributed to
this man's congestive heart failure symptom.
Cardiovascular effects are also associated with these medications.
Orthostatic hypotension, i.e. dizziness upon arising or otherwise rapidly
changing posture, is common. A rapid heartbeat is often reported,
sometimes with palpitations. The medications can have deleterious effects
on an unhealthy heart, e.g. causing EKG (electrocardiogram) changes or
arrhythmias (disturbances in cardiac rhythm or conduction); or, rarely,
worsening or precipitating angina or heart failure or precipitating a
myocardial infarction (heart attack). These cardiac effects may eliminate
the tricyclics from consideration for some patients, although with close
ongoing monitoring they may often be employed to good effect. A
thorough evaluation of their safety in the presence of reported history of
cardiac disease, especially a cardiac conduction defect, is always warranted
and may involve a referral for a consultation with a cardiologist. In all
patients from middle adulthood, it is prudent to obtain an EKG prior to
treatment and with dosage increases beyond a certain extent.
Tricyclic antidepressants are now the leading cause of death by drug
overdose in the United States.
What are the preliminaries to starting on a tricyclic? A thorough medical
screening including bloodwork is required to be sure that a medical illness
is not being mistaken for the psychiatric diagnosis. It is crucial as well to
determine whether you have the types of cardiac conduction disease which
would make the use of a tricyclic dangerous. These can be detected with an
EKG, which should be a routine precursor to beginning on a tricyclic for
patients over 40 years of age or anyone with a history of heart disease.
When doubts about the safety of these drugs arise, a cardiology
consultation is prudent.
maine drug related mortality patterns ( mentioned aventyl) Amertiptyline
is one of the worst drugs that cause death.