Sandbox:Mitra: Difference between revisions

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Revision as of 16:27, 17 June 2021

  • Efficacy: Low
    • Sinus rhythm is maintained in <20% of patients
    • Symtoms are reduced in >=20%.
Adverse effects
  • Bradycardia
  • Hypotension
  • Edema
Contraindications
  • Bradycardia
  • Hypotension
  • Heart failure with depressed ejection fraction


Contraindications
Precautions during treatment


[1]

[2]

Books by Psychologists and Psychiatrists

  • Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). Cognitive therapy of depression. New York: Guilford.
  • Burns, David D. (1999). Feeling Good : The New Mood Therapy. Avon.
  • Griffin, J., Tyrrell, I. (2004) How to lift Depression – Fast. HG Publishing. ISBN 1-899398-41-4
  • Jacobson, Edith: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
  • Klein, D. F., & Wender, P. H. (1993). Understanding depression: A complete guide to its diagnosis and treatment. New York: Oxford University Press.
  • Kramer, Peter D. (2005). Against Depression. New York: Viking Adult.
  • Plesman, J. (1986). Getting off the Hook, Sydney Australia. A self-help book available on the internet.
  • Rowe, Dorothy (2003). Depression: The way out of your prison. London: Brunner-Routledge.
  • Sarbadhikari, S. N. (ed.) (2005) Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends. Hauppauge, Nova Science Publishers. ISBN 1-59454-114-0.
  • Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
  • Bieling, Peter J. & Anthony, Martin M. (2003) Ending The Depression Cycle. New Harbinger Publications. ISBN 1572243333
  • For books on male depression, see Terrence Real

Historical Account

  • Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0

af:Kliniese depressie ar:الاكتئاب عند الإنسان bs:Klinička depresija ca:Depressió cs:Deprese (psychologie) da:Depression de:Depression et:Depressioon el:Κλινική κατάθλιψη eo:Deprimo ko:우울증 hr:Klinička depresija id:Depresi it:Depressione (malattia) he:דיכאון ku:Klînîk depresyon la:Depressio (psychiatria) lt:Depresija hu:Depresszió ms:Kemurungan nl:Klinische depressie nds-nl:Depressie (psychologie) no:Depresjon (sykdom) nn:Depresjon oc:Depression uz:Klinik depressiya simple:Depression (illness) sk:Depresia (psychológia) sr:Klinička depresija fi:Masennus sv:Depression uk:Депресія (медицина) yi:קלינישע דעפרעסיע

Template:WH Template:WS

Medical Therapy

Antidepressant drugs include selective serotonin reuptake inhibitors, such as escitalopram oxalate (Lexapro), citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primary medications considered for patients, having fewer side effects than the older monoamine oxidase inhibitors (MAOIs).

The effect size is very small for moderate depression but increased with severity reaching the NICE criteria for 'clinical significance' for very severe depression.[3] This result is consistent with the earlier clinical studies where only patients with severe depression benefited from the treatment with a tricyclic antidepressant imipramine or from psychotherapy more than from the placebo treatment.[4][5][6] According to the STAR*D randomized controlled trial, about 50% of patients with major depression have a response and about 30% of have remission of symptoms with usage of citalopram.[7]

Bupropion (Wellbutrin, Zyban), an atypical antidepressant that acts as a norepinephrine and dopamine reuptake inhibitor, is also considered to be effective in the treatment of depression,[8] without sexual dysfunction or sexual side effects[9] and without weight gain. Bupropion has also been shown to be more effective than SSRIs at improving symptoms such as hypersomnia and fatigue in depressed patients.[10]

Measurement-based care, which guides mediation based on serial measurement of psychometric testing, improves outcomes according to randomized controlled trials[7][11].

Predictors of a response to treatment

Severity of depression

The effectiveness is antidepressants may[12] or may not[13][14] depend on the severity of a patient's depression. This relationship may be due to the declining effect of placebo among more severely depressed patients.

The effectiveness of antidepressants depending on severity of depression[12]
American Psychiatric Association
classification of severity[15]
Hamilton Depression Rating Scale
(HDRS)
Number needed to treat[12] Clinical significance
(NICE)[16]
Mild to moderate < 19 16 No
Severe 19 - 22 11 No
Very severe > 22  4 Yes
Genetic variations

Variations in the GRIK4 (glutamate receptor, ionotropic, kainate 4 protein) and HTR2A (5-hydroxytryptamine receptor) genes predict response to citalopram.[17]

Treatment failure

Treatment after monotherapy failure
(VAST-D Study)[18]
Intervention Outcome
Medication Mode final dose Remission % Quit 2˚ ADRs (%)
Switch medications
Bupropion SR 200 mg twice daily 22.3% 10%
Augment medications
Aripiprazole 10 mg 29% 5%
Bupropion SR 300 mg daily 27% 7%

After starting medications, treatment should be switched if there is no response within one month.[19]

When treated with monotherapy for depression, approximately 30% of patients have remission of symptoms while 50% have a response to medications.[7]

For patients with inadequate response, randomized controlled trials provide guidance.[18][20]

  • The original VAST-D trial, that did not include aripiprazole, confirms that augmenting with bupropion is the most effective of options other than augmentation with aripiprazole. In this trial, either adding sustained-release bupropion ("bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6") or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients (bupropion may be more effective than buspirone)[20], while switching medications can achieve remission in about 25% of patients[21]. Alternatively, "extended-release venlafaxine, the starting daily dose of 37.5 mg for 7 days was increased to 75 mg from day 8 to 14, to 150 mg from day 15 to 27, to 225 mg from day 28 to 41, to 300 mg from day 42 to 62, and to 375 mg from day 63 onward."[21]
  • The PReDICT trial found that among patients who initially were treated with either an SSRI or CBT, remission was increased when the opposite treatment (CBT or SSRI) was added to non-remitters[22].
  • The newer VAST-D trial found that augmentation with aripiprazole is effective.[18] The dose of aripiprazole was 2 mg of with titration to 5, 10, or 15 mg daily as guided by measurement-based care using the PHQ-9.[18] However, aripiprazole led to more adverse drug reactions including somnolence, akathisia, and weight gain. The second most effective was augmentation with buproprion starting at 150 mg sustained release to 300 mg or 400 mg daily as guided by measurement-based care using the PHQ-9.
Treatment after SSRI (citalopram) failure
(STAR*D Studies)
Intervention Outcome
Medication Mean final dose Remission % Quit 2˚ ADRs (%)
Switch meds (NEJM 2006; PMID: 16554525[21])
Bupropion SR 283 mg 21% 27%
Sertraline (SSR) 136 mg 18% 21%
Venlafaxine ER (SNRI) 194 mg 25% 21%
Augment meds (NEJM 2006; PMID: 16554526[20])
Bupropion SR 268 mg 30% 13%
Buspirone 41 mg 30% 21%

The STAR*D trial has reported the frequency of re-emergence of suicidality for different second levels of treatment.[24]

In level 3 of the STAR*D trials, patients who had failed two trials of a second-generation antidepressant, tended to better with nortriptyline than mirtazapine.[25]

Aripiprazole, originally introduced as an atypical antipsychotic agent, is approved as an adjunct to other antidepressants.[26]

Stopping medications

Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four to months to prevent the chance of recurrence.[19] For patients that have chronic depression, medication may need to be continued for the remainder of their life.


Patients should be treated indefinitely if they have "three or more prior major depressive episodes or who have chronic major depressive disorder should proceed to the maintenance phase of treatment after completing the continuation phase."[19]


Distinguishing the Jugular Venous Pulse frm the Carotid Pulse
Feaure Internal Jugular Vein Carotid Artery
Appearance of pulse Biphasic Monophasic
Response to inspiration Inspiration generally decreases the pressure (the height of column decrease and troughs become more prominent) No respiratory change


Pulpabillity Not palpable (exception: severe TR) Palpable
Effect of pressure



Table

Therapies to maintain sinus rhythm
Treatment Efficacy Adverse effects Contraindications Precausions
Drug therapy
Beta-blockers
  • Low
  • Sinus rhythm is maintained in <20% of patients
  • Symptoms are reduced in >=20% of patients
  • Fatigue
  • Bradycardia
  • Monitor for bradycardia
  • Bradycardia
  • Hypotension
  • Monitor for bradycardia
Nondihydropyridine Calcium Channel Blockers:
  • Low
  • Sinus rhythm is maintained in <20% of patients
  • Symptoms are reduced in >=20% of patients
  • Edema
  • Bradycardia
  • Hypotension
Flecainide
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • Uncommon
  • Proarrhythmia risk in patients with structural heart disease
  • Structural heart disease (proarrhythmia risk)
  • Evaluate for ischemic heart disease before initiation of therapy
Propafenone
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • Dysgeusia
  • Structural heart disease (proarrhythmia risk)
  • Evaluate for ischemic heart disease before initiation of therapy
Quinidine
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • Gastrointestinal side effects
  • QT prolongation
  • Monitor for QT prolongation, polymorphic ventricular tachycardia
Disopyramide
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • Antimuscarinic effects
  • Urinary retention
  • QT prolongation
  • Heart failure
  • Monitor for QT prolongation,
Dronendrone
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • Uncommon
  • Heart failure
  • Monitor for:
    • Fluid retention
    • Hepatitis
Dofetilide
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • QT prolongation
  • QT prolongation
  • Advanced renal disease
  • Monitor for QT prolongation (should be initiated in hospital)
Sotalol
  • Moderate
  • AF is prevented or reduced in 50-70% of patients
  • QT prolongation
  • Fatigue
  • Bradycardia
  • Hypotension
  • QT prolongation
  • Advanced renal disease
  • Bradycardia
  • Monitor for QT prolongation
Amiodarone
Interventional procedures
Catheter ablation
Surgery (Maze procedure)











Resident
Survival
Guide

Acute Coronary Syndrome Chapters

Heart Attack Patient Information

Unstable Angina Patient Information

Overview

Classification

Unstable Angina
Non-ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction

Causes

Differential Diagnosis

Treatment

AHA/ACC Guidelines for Acute Coronary Syndrome

Guideline for Risk Stratification in ACS
Guideline for Pre-Hospital Evaluation and Care
Guidelines for Initial Management of ACS
Guidelines for Patients with Atrial Fibrillation Complicating ACS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]; Tarek Nafee, M.D. [3]; Sabawoon Mirwais, M.B.B.S, M.D.[4]

Synonyms and keywords: ACS

Overview

Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST-elevation myocardial infarction (30%), non ST-elevation myocardial infarction (25%), or unstable angina (38%). These types are named according to the appearance of the electrocardiogram. There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome.

ACS should be distinguished from stable angina, which is chest pain which develops during exertion and resolves at rest. New onset angina however should be considered as a part of acute coronary syndrome, since it suggests a new problem in a coronary artery.Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. Cardiac chest pain can also be precipitated by anemia, bradycardias or tachycardias.

Classification

Acute coronary syndrome may be classified as follows:

Symptoms

The signs and symptoms of acute coronary syndrome include:

Pathophysiology

For more information on atherosclerotic plaque, click here.

The pathophysiology of acute coronary syndromes depends on coronary atherosclerotic plaque which includes:

Initiation and Progression of Coronary Atherosclerotic Plaque

Plaque Vulnerability

The plaque vulnerability depends on the following factors:[27]

Pathogenesis

The pathogenesis of acute coronary syndrome depends on:

Following plaque rupture or endothelial erosion, the subendothelial matrix is exposed to the circulating platelets, which get activated leading to thrombus formation. Two types of thrombi can form:

  • White clots: Platelet-rich clots which partially occludes the artery
  • Red clots: Fibrin rich clots superimposed on white clots and cause total occlusion of the artery

Risk Factors

Common risk factors in the development of acute coronary syndrome are:[28]

Diagnosis

High-sensitivity Cardiac Troponin (hs-cTn)

99th percentile of a healthy reference population
(recommended cut-off)
Turnaround time Name and manufacturer FDA Approval?
Troponin T
hs-cTnT
14 ng/L[29] 18 minutes[30] Elecsys
(Roche Diagnostics)
Troponin I
hs-cTnI
26.2 ng/L[29] ARCHITECTSTAT
(Abbott Laboratories)

Clinical Implications of High-sensitivity Cardiac Troponin Assays

Compared with standard cardiac troponin assays, high-sensitivity assays:
Have higher negative predictive value for acute MI.
Reduce the “troponin-blind” interval leading to earlier detection of acute MI.
Reduce the “troponin-blind” interval leading to earlier detection of acute MI.
Are associated with a 2-fold increase in the detection of type 2 MI.
Levels of high-sensitivity cardiac troponin should be interpreted as quantitative markers of cardiomyocyte damage

(i.e. the higher the level, the greater the likelihood of MI):

Elevations beyond 5-fold the upper reference limit have high (>90%) positive predictive value for acute type 1 MI.
Elevations up to 3-fold the upper reference limit have only limited (50–60%) positive predictive value for acute MI

and may be associated with a broad spectrum of conditions.

It is common to detect circulating levels of cardiac troponin in healthy individuals.
Rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage

(the more pronounced the change, the higher the likelihood of acute MI).

Adapted from European Heart Journal (2016) 37, 267–315



Available high sensitivity troponin assays:

  • Troponin T: Elecsys by Roche Diagnostics
  • Troponin I: ARCHITECTSTAT by Abbott Laboratories

When both tests have sensitivity of > 99%, cTnT can exclude infarction in more patients with a sensitivity of 90% according to meta-analysis.

The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)[29].

High sensitivity troponin levels have reduced predictive value when prevalence is low.

Clinical Prediction Rules

Clinical prediction rules can help diagnose:

  • HEART risk score (History, EKG, Age, Risk factors, and troponin) is the only one of these three prediction rules designed for use prior to diagnosis
  • GRACE risk score incorporates 8 findings
  • TIMI risk score

Regarding the comparative performance of the prediction rules:

  • In the setting of acute chest pain, the HEART score may best predict complications according to a cohort study.
  • In the setting of NSTEMI, the GRACE risk score may best predict complications according to a cohort study. However, the HEART risk score was not assessed in this cohort.

Diagnostic Pathways

Clinical diagnostic pathways may help. The European Society of Cardiology recommends two pathways[31]:

The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA.

More recent strategies include:

  • Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection.
  • Single cTnI measurement, combined with low-risk clinical prediction rule[34]

Differential Diagnosis

Diagnosis of ACS is initiated by a clinical suspicion based on a thorough history of the patient's symptoms. Subsequently, confirmatory tests should be ordered to confirm the diagnosis, identify the specific cause of ACS, or to rule out other possible differentials. In some circumstances, utilizing a clinical prediction tool may be beneficial in guiding the clinician's diagnosis. View the page on diagnosis using the clinical prediction rule for ACS for more detail. Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows:

Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Cardiovascular Acute Coronary Syndrome + + + + + + + + + + + Palpitations

Sweating

Aortic Dissection + + + - + + - + •Pain maximal upon onset •Pain difficult to treat with opiates

Weak pulse in one arm compared to other

Syncope

•Symptoms similar to stroke

Smoking

Brugada Syndrome No chest pain + Syncope

Cardiac arrest

ST-segment elevation

•F/H of sudden cardiac death

Takotsubo carditis Sudden onset of chest pain mimicking myocardial infarction + + + + + - •Extreme emotional or physical stresssyncope

•Women>men

ST segment elevation

Left ventricular apical ballooning on echo

Normal coronary arteries

Pericarditis + + + •Relieving factor: Sitting up and leaning forward

•Aggravating factor: Lying down and breathing deep

+ + + + + + + •Other causes:Malignancy, autoimmune disorders, chest trauma

Pericardial friction rub

Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Pulmonary Pleuritis
(pleurisy)
+ + + + Aggravating factor: Deep breathing + + + + + + •Other causesPulmonary embolism, malignancy, autoimmune diseases
Pulmonary Embolism + •Aggravating factors: Deep breathing, coughing, eating, bending and stooping + + + •Other causes: Immobility, pregnancy, oral contraceptive pills
Pneumonia + + + + + + •Complications: Sepsis, ARDS, Lung abscess
Gastrointestinal GERD + + + •Other symptoms: Hoarseness, Dry cough at night, Sensation of lump in throat etc
Esophageal Spasms + + + + + + + • Risk factors: Anxiety or depression and drinking wine, very hot or cold foods
Esophagitis + + + + + + + • Causes: Hiatal hernia, infection, medications, radiation therapy
Gastritis + + + + + + + • Causes: H.pylori infection, bile reflux, alcohol use, alcohol use
Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Musculoskeletal Muscle sprain/Spasm + + + + • Causes: Over use, dehydration, electrolyte abnormalities
Costochondritis + + + + + + + + + + + • Risk factors: Rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome
Rib fracture/Trauma + + + + + + + + + + • Complications: Pneumothorax, hemothorax, surgical emphysema
Psychiatry Anxiety (Panic Attack) Chest tightness + + • Other symptoms: Palpitations, trembling, sweating, choking, light headed, hot or cold flashes.


The following table summarizes the significant history, and diagnostic test findings that will help differentiate the acute coronary syndromes from one another, as well as from other coronary artery diseases:

Acute Coronary Syndromes History and Symptoms Pathology Diagnostic tests Treatment Complications Prognosis
Chest pain Duration of Chest pain Coronary Artery Plaque Cardiac Biomarkers
(e.g.CK-MB, Troponins)
EKG Findings Medical Therapy Reperfusion
(e.g. PCI, CABG, or Medical)
At Rest Exertion
Unstable Angina + + <30 minutes Partial occlusion Erosion

or

Rupture

(39%)

Normal •Normal EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

+ Arrhythmias

Congestive heart failure

Hypotension

New mitral regurgitation

MI

•Sudden death

•1 year mortality rate is 1.7%
NSTEMI + + >30 minutes Partial or complete occlusion Rupture

(56%)

or

Erosion

Elevated •No EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

New left bundle branch block

+ + Arrhythmias

Congestive heart failure

Hypotension

New mitral regurgitation

Ventricular aneurysms

•Sudden death

•1 year mortality rate is 24.4%

•30 day mortality rate is about 2%

STEMI + + >30 minutes Complete occlusion Rupture

(50%-75%) or

Erosion

Elevated •ST elevation in at least 2

contiguous leads in V2-V3


•ST depression in at least

two precordial leads V1-V4


•ST depression in several

leads plus ST elevation in

lead aVR (suggestive of occlusion of the left main or proximal LAD artery)


+ + Reinfarction

Arrhythmias

Left ventricular aneurysm

Pseudoaneurysm

rupture of papillary muscle,

interventricular septum and LV free wall

•Sudden death

•30 day mortality rate is

1.1% in <45 yrs and 20.4% in >75 yrs patients

Other Coronary Artery Diseases
Chronic stable angina - + ≤ 5 minutes Severely narrowed

coronary vessels

Stable plaque Normal •Normal EKG in 50% of cases

•Down sloping, up sloping or

horizontal ST segment depression

•T wave inversion

+ Heart failure •Estimated annual mortality rate is 0.9%-1.4%

•Annual incidence of non-fatal MI between 0.5%-2.6%

•1 year mortality rate is 1.3%

Prinzmetal's angina •Occur at rest

(Mid night to early morning)

•Not associated with exertion

5-30 minutes Coronary artery vasospasm - Normal •Transient ST segment elevation + Arrhythmias

MI

•5 year survival is excellent (90%-95%)


Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain


Cardiac Pulmonary Vascular Gastrointestinal Orthopedic Other
Myopericarditis

Cardiomyopathiesa

Pulmonary embolism Aortic dissection Esophagitis, reflex or spasm Musculoskeletal disorders Anxiety disorders
Tachyarrhythmias (Tension)-Pneumothorax Symptomatic aortic aneurysm Peptic ulcer, gastritis Chest trauma Herpes zoster
Acute heart failure Bronchitis, pneumonia Stroke Pancreatitis Muscle injury/inflammation Anemia
Hypertensive emergencies Pleuritis Cholecystitis Costochondritis
Aortic valve stenosis Cervical spine pathologies
Tako-Tsubo cardiomyopathy
Coronary spasm
Cardiac trauma
Bold = Common and/or important differential diagnoses

aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort

Treatment

Coronary Angiography

Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a GRACE score more than 140) patients.

Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes

Recommendations Class

of Recommendations

Level

of Evidence

Early initiation of beta-blocker treatment is recommended

in patients with ongoing ischemic symptoms and without contraindications.

I B
It is recommended to continue chronic beta-blocker therapy,

unless the patient is in Killip class III or higher.

I B
Sublingual or i.v. nitrates are recommended to relieve angina;a intravenous treatment is recommended

in patients with recurrent angina, uncontrolled hypertension or signs of heart failure.

I C
In patients with suspected/confirmed vasospastic angina, calcium channel blockers and

nitrates should be considered and beta-blockers avoided.

IIa B
aShould not be administered in patients with recent intake of sildenafil or vardenafil (< 24 h) or tadalafil (< 48 h).

Prevention

Primary Prevention

The primary prevention strategies include:

  • Dietary modifications:
  • Physical exercise
  • 30 minutes of moderate exercise

Secondary Prevention

The secondary prevention strategies include:

References

  1. LastName, FirstName (2013). Diagnostic and statistical manual of mental disorders : DSM-5. Arlington, VA Washington, D.C: American Psychiatric Association,American Psychiatric Association. ISBN 978-0-89042-554-1.
  2. ....
  3. Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration" (htm). PLoS Medicine. Retrieved 2008-02-26.
  4. Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP (1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Arch. Gen. Psychiatry. 46 (11): 971–82, discussion 983. PMID 2684085.
  5. Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". J Consult Clin Psychol. 63 (5): 841–7. PMID 7593878.
  6. Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J (1991). "Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program". Am J Psychiatry. 148 (8): 997–1008. PMID 1853989.
  7. 7.0 7.1 7.2 Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L; et al. (2006). "Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice". Am J Psychiatry. 163 (1): 28–40. doi:10.1176/appi.ajp.163.1.28. PMID 16390886.
  8. Fava M, Rush AJ, Thase ME, Clayton A, Stahl SM, Pradko JF, Johnston JA. (2005). "15 years of clinical experience with bupropion HCl: from bupropion to bupropion SR to bupropion XL". Prim Care Companion J Clin Psychiatry. 7 (3): 106–113. PMID 16027765.
  9. For the review, see: Clayton AH (2003). "Antidepressant-Associated Sexual Dysfunction: A Potentially Avoidable Therapeutic Challenge". Primary Psychiatry. 10 (1): 55–61.
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CME Category::Cardiology