Acetylsalicylic acid

Mechanism

At high aspirin doses (above 1 g/day), vasodilator prostaglandins are suppressed, weakening amlodipine's antihypertensive effect. At cardioprotective doses (75–100 mg/day), the effect is minimal.

Symptoms

Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At anti-inflammatory aspirin doses, monitor blood pressure and increase amlodipine if needed.

Mechanism

Additive ulcerogenic effect with oral budesonide (used in inflammatory bowel disease). Inhaled forms have minimal systemic effect.

Symptoms

Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.

Management

Inhaled budesonide for asthma or COPD requires no special measures. For oral therapy (Crohn's disease, ulcerative colitis): PPI cover with pantoprazole, cardioprotective aspirin no more than 100 mg/day.

Mechanism

At analgesic doses (above 1 g/day), aspirin suppresses vasodilator prostaglandins and weakens the ACE-I's hypotensive effect. At cardioprotective doses (75–100 mg), the effect is minimal.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase captopril if needed. Alternative analgesic: paracetamol.

Mechanism

Celecoxib is a selective COX-2 inhibitor and does not displace aspirin from COX-1 (unlike ibuprofen/naproxen). Aspirin's antiplatelet effect is preserved. Additive GI bleeding risk persists.

Symptoms

Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.

Management

The combination is acceptable. Aspirin's cardioprotective effect is preserved. PPI cover with pantoprazole is mandatory in chronic celecoxib therapy. Check blood pressure and creatinine every 3 months.

Mechanism

Old experimental data suggested NSAIDs combined with fluoroquinolones increase CNS excitability and seizure risk (via GABAergic suppression). Clinical data are very limited.

Symptoms

Mostly asymptomatic. In patients with prior epilepsy or head injury: rare seizure cases.

Management

The combination is acceptable in patients without prior epilepsy. In epilepsy or eating disorders: alternative antibiotics (a cephalosporin, nitrofurantoin) and paracetamol for analgesia.

Mechanism

Similar to ASA + fluvoxamine. SSRI-induced platelet dysfunction plus aspirin's antiplatelet effect – bleeding risk.

Symptoms

Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.

Management

The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants: mirtazapine or agomelatine.

Mechanism

Additive antiplatelet effect via different targets: aspirin irreversibly blocks platelet cyclooxygenase; clopidogrel inhibits the P2Y12 receptor. The combination raises bleeding risk 1.5- to 2-fold versus monotherapy.

Symptoms

Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.

Management

The combination (dual antiplatelet therapy) is standard after acute coronary syndrome or coronary stenting. Limit duration to 1–6 months based on thrombosis and bleeding risk. Aspirin 75–100 mg/day. Mandatory PPI cover with pantoprazole.

Mechanism

Additive ulcerogenic effect. Dexamethasone suppresses GI mucosal repair; aspirin blocks protective prostaglandins.

Symptoms

Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.

Management

For short dexamethasone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic glucocorticoid therapy, watch dyspepsia symptoms; consider stool occult blood testing as needed.

Mechanism

High aspirin doses can reduce renal digoxin clearance via prostaglandin-dependent renal blood flow suppression. The effect is clinically significant at analgesic aspirin doses (above 1 g/day), not cardioprotective ones.

Symptoms

Nausea, anorexia, visual disturbances (yellow-green halos around lights), arrhythmias at aspirin doses above 1 g/day.

Management

Cardioprotective aspirin doses are acceptable without adjustment. At high doses, check digoxin level at 1 week. For chronic analgesia on digoxin: paracetamol.

Mechanism

Diltiazem impairs platelet function via calcium channel blockade; aspirin is an antiplatelet. Mild additive bleeding risk, rarely clinically significant.

Symptoms

Usually asymptomatic. In patients with bleeding risk factors (peptic ulcer, older age): rare gum bleeding and epistaxis.

Management

Standard combination in ischaemic heart disease. Cardioprotective aspirin doses (75–100 mg) are acceptable without special measures. In patients with bleeding risk factors: PPI cover with pantoprazole.

Mechanism

Duloxetine (SNRI) depletes the platelet serotonin pool, impairing primary haemostasis. Additively with aspirin's antiplatelet effect: GI bleeding risk roughly doubles.

Symptoms

Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.

Management

The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.

Mechanism

High aspirin doses (above 1 g/day) weaken the hypotensive and cardioprotective effects of the ACE-I via vasodilator prostaglandin suppression. At cardioprotective doses (75–100 mg/day), the clinical effect is minimal.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high aspirin doses, monitor blood pressure and increase enalapril if needed. Alternative analgesic: paracetamol.

Mechanism

SSRIs block serotonin reuptake into platelets, impairing primary haemostasis. Additively with aspirin's antiplatelet effect: upper GI bleeding risk roughly doubles.

Symptoms

Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.

Management

The combination is acceptable at low aspirin doses (75–100 mg as cardioprotection). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.

Mechanism

Additive nephrotoxicity. Aspirin suppresses prostaglandin-dependent renal blood flow (at high doses); gentamicin causes direct tubulotoxicity.

Symptoms

Reduced urine output, rising creatinine. Symptoms appear earlier in older patients and chronic kidney disease.

Management

Cardioprotective aspirin doses (75–100 mg) do not require withdrawal. At high doses, check creatinine before and 3–5 days into gentamicin therapy. Ensure adequate hydration; consider switching to a less nephrotoxic antibiotic (a cephalosporin, carbapenem).

Mechanism

High aspirin doses displace glibenclamide from albumin binding and suppress hepatic gluconeogenesis. Hypoglycaemia risk at aspirin doses above 3 g/day.

Symptoms

Sweating, tremor, hunger, tachycardia, confusion. Severe cases: seizures and coma. Symptoms appear 1–2 days after starting high aspirin doses.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor glucose 4 times daily in the first week; reduce glibenclamide if needed.

Mechanism

High aspirin doses (above 1 g/day) weaken the ARB's antihypertensive effect via vasodilator prostaglandin suppression. At cardioprotective doses, the effect is clinically minor.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase losartan if needed. Alternative analgesic: paracetamol.

Mechanism

Meloxicam is preferentially COX-2 selective and weakly displaces aspirin from COX-1. Additive GI bleeding risk persists from the ulcerogenic effect of both drugs.

Symptoms

Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.

Management

Aspirin's cardioprotective effect is preserved better than with ibuprofen/naproxen. PPI cover with pantoprazole is mandatory in chronic meloxicam therapy. Alternative analgesic: paracetamol or celecoxib.

Mechanism

Glucocorticoids damage the gastric mucosa and suppress protective prostaglandin production. Aspirin compounds the risk of GI ulcer and bleeding.

Symptoms

Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood). Older patients and prior peptic ulcer disease: higher risk.

Management

For short methylprednisolone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic therapy, watch dyspepsia symptoms; consider stool occult blood testing if needed.

Mechanism

Similar to ASA + methylprednisolone. Prednisolone + antiplatelet – additive risk of GI ulcer and bleeding.

Symptoms

Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood). Older patients and prior peptic ulcer disease: higher risk.

Management

For short prednisolone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic therapy, watch dyspepsia symptoms carefully.

Mechanism

High aspirin doses (above 1 g/day) may reduce the ARB's antihypertensive effect via vasodilator prostaglandin suppression. Cardioprotective doses (75–100 mg) are clinically minor.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase telmisartan if needed. Alternative analgesic: paracetamol.

Mechanism

Aspirin displaces valproate from albumin binding and suppresses its metabolism. The free valproate fraction rises, raising neurotoxicity risk (tremor, sedation, hyperammonaemia).

Symptoms

Tremor, drowsiness, nausea, confusion. Severe cases: hyperammonaemic encephalopathy. Symptoms appear within 1–2 weeks at high aspirin doses.

Management

Cardioprotective aspirin doses (75–100 mg) are usually acceptable. At high doses, check valproate level at 1 week. For chronic analgesia on valproate: paracetamol.

Mechanism

Analgesic aspirin doses weaken the ARB's antihypertensive effect via vasodilator prostaglandin suppression. Cardioprotective doses are clinically minor.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase valsartan if needed. Alternative analgesic: paracetamol.

Mechanism

Venlafaxine (SNRI) depletes the platelet serotonin pool, impairing primary haemostasis. With aspirin: additive GI bleeding risk.

Symptoms

Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.

Management

The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.

Mechanism

At high doses, aspirin weakens verapamil's antihypertensive effect via vasodilator prostaglandin suppression. At cardioprotective doses, there is no clinically significant effect.

Symptoms

Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.

Management

Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase verapamil if needed. Alternative analgesic: paracetamol.