Ramipril (Altace)




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  • PO:

Dose Adjustment

  • Hepatic
  • Renal

Adverse Effects

Allergic/Immunologic Adverse Effects

Anaphylaxis (see Anaphylaxis, [[Anaphylaxis]])

  • Epidemiology: xxx
  • Treatment: see Anaphylaxis, [[Anaphylaxis]]

Angioedema (see Urticaria-Angioedema, [[Urticaria-Angioedema]])

  • Epidemiology: occurs in 0.1-0.2% of ACE-Inhibitor treated patients
  • Physiology: class effect (common to all ACE inhibitors)
    • Mediated by bradykinins (and possibly by autoantibodies and complement activation)
  • Clinical
    • Time of Onset: onset can occur from hours-months after starting ACE-Inhibitor
      • However, most cases within hrs-1 week after starting ACE-Inhibitor
    • Lingual Edema (see Lingual Edema, [[Lingual Edema]])
    • Facial Edema (see Facial Edema, [[Facial Edema]])
  • Treatment
    • Airway Protection: as required
    • Antihistamines (see H1-Histamine Receptor Antagonists, [[H1-Histamine Receptor Antagonists]])
      • Diphenhydramine (Benadryl) (see Diphenhydramine, [[Diphenhydramine]]): 25-50 mg IV PRN
    • Epinephrine (see Epinephrine, [[Epinephrine]])
    • Corticosteroids (see Corticosteroids, [[Corticosteroids]])
    • Icatibant (Firazyr) (see Icatibant, [[Icatibant]])
    • Withdrawal of ACE-Inhibitor: rechallenge is contraindicated

Cardiovascular Adverse Effects

Hypotension (see Hypotension, [[Hypotension]])

  • Physiology: class effect (common to all ACE inhibitors)

Endocrinologic Manifestations

Hypoaldosteronism (see Hypoaldosteronism, [[Hypoaldosteronism]])

  • Physiology: class effect (common to all ACE inhibitors)

Gastrointestinal Adverse Effects

Elevation of Hepatic Transaminases with Hepatocellular Injury (see Drug-Induced Hepatotoxicity, [[Drug-Induced Hepatotoxicity]])

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Pulmonary Adverse Effects

Cough (see Cough, [[Cough]])

  • Epidemiology: occurs in 5-20% of treated patients
  • Physiology: class effect (common to all ACE inhibitors)
    • Likely related to accumulation of kinins and substance P (which are usually degraded by ACE and other endopeptidases)
  • Clinical: dry cough with onset typically wihtin the first few weeks of therapy (although some cases do not present with cough until months later)
  • Treatment: 50% of cases with cough ultimately need to have ACE-I discontinued -> cough usually stops within 4 days of discontinuation of ACE-I
    • Rechallenge with ACE-I is not recommended, as cough will usually recur
    • However, since ARB’s have much lower incidence of cough, one of these may be substituted

Drug-Induced Pulmonary Eosinophilia (see Drug-Induced Pulmonary Eosinophilia, [[Drug-Induced Pulmonary Eosinophilia]])

  • Physiology: class effect
    • Associated Agents
      • Captopril (see Captopril, [[Captopril]])
      • Fosinopril (see Fosinopril, [[Fosinopril]])
      • Perindopril (Coversyl, Coversum, Preterax, Aceon) (see Perindopril, [[Perindopril]])

Exacerbation of Bronchospasm (see Obstructive Lung Disease, [[Obstructive Lung Disease]])

  • Epidemiology: very rare
  • Physiology: class effect (common to all ACE inhibitors)

Renal Adverse Effects

Acute Kidney Injury (AKI) (see Acute Kidney Injury, [[Acute Kidney Injury]])

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Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]])

  • Physiology: class effect (common to all ACE inhibitors)
    • Due to drug-induced hypoaldosteronism (see above)

Rheumatologic Adverse Effects

Drug-Induced Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus, [[Systemic Lupus Erythematosus]])

  • Epidemiology: low-moderate risk of developing drug-induced SLE
  • Physiology: class effect (common to all ACE inhibitors)


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