Psychopharmacology andCardiovascular Disease.Your Heart And Mind Are Connected.Psychiatric Disorders and Cardiovascular System .Cardiac response to acute stress .Heart disease and depression are closely linkedCardiovascular Side Effects of Psychotropic Drugs
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2. Greatest burden of disease is from mental disorders, cardiovascular diseases and cancer
3. In recent years , psychological factors have been
reported to be tightly linked to CVD.
The link is bidirectional in that psychological factors
may be common in certain CVDs and portend worse
outcomes, or psychological conditions may pre-exist and
precede CVD.
Your Heart And Mind
Are Connected
4. Furthermore, treatment for mental
health disorders can present CV risk due
to side effects of the drugs or
interactions with other medications.
5. Rates of cardiovascular morbidity and
mortality in psychiatric patients are higher
than in the general population
6. (World Psychiatry 2017;16:163–180)
This large-scale meta-analysis confirms that severe
mental illness (SMI) patients have significantly increased
risk of CVD and CVD-related mortality,
and that elevated body mass index, antipsychotic use,
and CVD screening and management require urgent
clinical attention
8. P e r s o n a l i t y a n d C a r d i o v a s c u l a r D i s e a s e
Coronary-prone personality
9. Heart patients considered "chronically distressed" (Type D personality)
may have a higher risk of recurrent cardiac events.
Type D personality was also associated with higher risk of future
psychological problems such as depression or anxiety in heart patients.
10. Mediated through increases in circulating catecholamines, increased myocardial
oxygen demand, coronary vasospasm, and increased platelet aggregability, anger
can cause transient ischaemia, disruption of vulnerable plaques, and increased
thrombotic potential.
These changes can then result in myocardial or cerebral
ischaemia or malignant arrhythmias
Anger and CVD
11. Cardiac response to acute stress:
cardiovascular outcomes related to acute episodes of anxiety.
12. The Pathophysiological Effects of Acute Psychosocial Stress
Piña, I.L. et al. J Am Coll Cardiol. 2018;71(20):2346–59.
Stimulation of the SNS leads to a variety of physiological effects, affecting HR, BP, and
coronary vascular endothelium.
The outcomes of acute stress result in myocardial ischemia, arrhythmias, and increasing
vulnerability of plaques.
13.
14. Heart disease and depression are closely linked.
People with depression are more likely to suffer from heart disease.
People with heart disease are more likely to suffer from depression.
15. The prevalence of depression in patients with CVD is 3-fold
higher than in the general population
Depression
should be
recognized as a
major risk factor
for CAD
Depression is
commonly
present in
patients with
CAD and can
increase the
development of
MI, stroke,
sudden death,
and AF
16. There are shared pathophysiological mechanisms between
HF and depression : a chicken-and-egg dilemma
20. Cardiovascular
Side Effect
Profile of
Psychotropic
Drugs
0 = no or minimal effect;
+=mild effect;
++= moderate effect;
+++= severe effect
Due to their efficacy and their
established record of safety, SSRIs are
the first-line treatment for depression
and anxiety in patients with cardiac
disease.
Antipsychotics can be safely used in
cardiac patients, with atypical agents
considered first line treatment.
Efforts should be made to minimize
metabolic side effects in patients
with CAD or CHF.
Antipsychotic agents also carry a
risk of prolonged QTc intervals and
caution should be exercised in this
regard.
Selective serotonin reuptake inhibitors
Serotonin and norepinephrine reuptake inhibitors
Tricyclic antidepressants
22. An algorithm for lowering the risk of cardiac arrhythmia during treatment with psychotropic medications.
When a class B or B* drug (Table 2) is chosen, assessment of the cardiac risk profile is recommended. If cardiac risks are
identified—the cardiac risk factors should be optimized and/or a drug with a more favourable risk profile should be
chosen. Re-evaluation of the ECG and symptoms should take place within 1 to 2 weeks after ( 5 half lives) initiation of
treatment with class B/B* drugs.
23. Clinical features associated with increased risk of TdP
Prolonged QTc interval. Torsades de pointes. (syncope, seizure, sudden death)
Health QTc 400ms,
Upper M=450ms
F=460ms
>500ms or Δ60ms
risk for TdP
26. Propensity for weight gain for selected psychotropic medications.
Medications and those who take them
exhibit considerable variability in liability for weight gain.
29. CON: concomitant prescription of cardiovascular and psychotropic drugs; C: cardiovascular drug
prescription; P: psychotropic drug prescription; NO: no prescription of cardiovascular and psychotropic
drugs. Ozturk Z, Turkyilmaz A. Concomitant prescription of psychotropic and cardiovascular drugs in elderly patients. Psychiatry Clin
Psychopharmacol 2017;27:374–9.
Prescription of cardiovascular and psychotropic drugs in elderly patients, stratified by age.
CON
C
P
NO
The rate of cardiovascular or
psychiatric prescription drugs
was higher in the oldest age
group (80+ years) compared
with the other age groups.
NO
P
C
CON
30. Pathways of Metabolism and Excretion
Phase I
Metabolism
(Oxidation)
• Most Psychiatric
Medications
• CYP450
Phase II
Metabolism
(Glucuronidation)
• Lorazepam, oxazepam,
temazepam
• Desvenlafaxine, paliperidone
Renal & Biliary
Excretion
• Exclusively renally excreted
(no hepatic metabolism):
• Lithium
• Gabapentin
• Pregabalin
• Topiramate
Ferrando SJ et al. 2010
Pharmacokinetics of Psychotropic Drugs
31. Remember
Inhibitors INCREASE the effectiveness of another drug
(substrate)metabolized by cytochrome P450
Inducers DECREASE effectiveness
Psychotropic
&
Cardiovascular
drugs behave
as substrates,
inhibitors and
inducers of
human
cytochrome
P450
For CYP450-mediated
metabolisms
33. Platelets will release serotonin in response to vascular damage/ injury. This promotes the
pro-thrombotic cascade — promoting vasoconstriction and platelet aggregation.
However, platelets do not create serotonin and rely on serotonin transporters (SERT).
SSRIs inhibit the serotonin transporter, which is responsible for the uptake of serotonin into
platelets. It could thus be theorized that SSRIs would deplete platelet serotonin, leading to
a reduced ability to form clots and a subsequent increase in the risk of bleeding.
SSRIs have been implicated in a modest increase risk of Upper GI bleeds :
proposed mechanism
34.
35. While many psychiatric medications are safe for use in
patients with cardiac disease, physicians need to be
aware of and monitor for potential side effects that
may be specific to individual classes.
The presence of heart disease should not preclude
necessary treatment of psychiatric comorbidity given the
links between cardiac disease and psychiatric illness
Optimizing
psychotropic
medication
use