In a typical adult patient without other QT‑prolonging drugs or electrolyte abnormalities, does rosuvastatin (Crestor) increase the QTc interval?

Does Rosuvastatin (Crestor) Increase QTc?

Yes, rosuvastatin modestly increases the QTc interval by approximately 6–7 ms on average, but this effect does not appear to cause clinically significant arrhythmias or increase mortality when used as monotherapy in typical patients without additional risk factors. 1, 2

Evidence for QTc Prolongation

The most recent randomized controlled trial (2025) demonstrated that rosuvastatin increased QTc by 6.57 ms from baseline, compared to a 0.83 ms decrease with atorvastatin. 1 Importantly, 62.7% of rosuvastatin-treated patients experienced some QTc increase versus 46.6% on atorvastatin, and rosuvastatin increased the risk of newly emerged QT prolongation by 42% (95% CI 1.10–1.85). 1

Real-world data from 2023 corroborated these findings, showing an association between rosuvastatin use and QT prolongation (OR 1.30,95% CI 1.21–1.39), while atorvastatin showed no such association (OR 0.98,95% CI 0.89–1.07). 2 Laboratory studies using human-induced pluripotent stem cell–derived cardiomyocytes confirmed that rosuvastatin affects sodium and calcium channel activities in addition to blocking hERG potassium channels. 2, 3

Clinical Significance and Safety Profile

Despite the measurable QTc increase, rosuvastatin monotherapy does not appear to increase arrhythmia risk or all-cause mortality. 1, 2 The 2025 trial found no correlation between rosuvastatin and severe QT prolongation (RR 1.23,95% CI 0.74–2.06, p=0.426), and nationwide claims data showed no association with increased mortality (HR 0.95% CI 0.89–1.01). 1, 2

The QTc increase of ~6–7 ms falls well below the 60 ms threshold that signals high risk for torsades de pointes. 4, 5 For context, the American College of Cardiology defines critical QTc prolongation as >500 ms or an increase >60 ms from baseline—thresholds that rosuvastatin monotherapy does not approach. 4, 5

When to Exercise Caution

The primary concern arises when rosuvastatin is combined with other QT-prolonging medications, as additive effects may occur. 1, 3 The 2025 trial explicitly noted it did not assess rosuvastatin combined with other QT-prolonging drugs, and mechanistic studies emphasize caution with polypharmacy. 1, 3

High-Risk Scenarios Requiring Monitoring:

• Concomitant QT-prolonging drugs: antiarrhythmics (amiodarone, sotalol), macrolide or fluoroquinolone antibiotics, antiemetics (ondansetron), antipsychotics (haloperidol, ziprasidone), or certain antidepressants 6, 4
• Electrolyte abnormalities: hypokalemia (<4.0 mEq/L) or hypomagnesemia (<2.0 mg/dL) 6, 4, 5
• Baseline QTc >460 ms in females or >450 ms in males 4, 5
• Structural heart disease: heart failure with ejection fraction <40%, acute coronary syndrome, or significant left ventricular hypertrophy 6, 4
• Age >65 years, female sex, or bradycardia <45 bpm 6, 4

Practical Management Algorithm

For Typical Patients (No Additional Risk Factors):

• No baseline ECG required before starting rosuvastatin 4
• Continue rosuvastatin without QTc monitoring 1, 2
• Educate patients to report palpitations, syncope, or dizziness 4

For Patients with 1–2 Risk Factors:

• Obtain baseline ECG and measure QTc using Fridericia's formula 4, 7
• Check serum potassium and magnesium before initiation 4, 7
• Review medication list for QT-prolonging drugs using crediblemeds.org 4, 7
• Repeat ECG 7–15 days after starting rosuvastatin if baseline QTc is 440–480 ms 4, 7

For Patients with ≥3 Risk Factors or Baseline QTc >480 ms:

• Consider alternative statin (atorvastatin shows no QTc effect) 1, 2
• If rosuvastatin is necessary, obtain cardiology consultation 4
• Correct electrolytes aggressively (potassium >4.5 mEq/L, magnesium >2.0 mg/dL) 4, 5
• Monitor ECG every 8–12 hours initially, then weekly 4

If QTc Increases to >500 ms or Δ>60 ms:

• Discontinue rosuvastatin immediately 4, 5
• Administer 2 g IV magnesium sulfate regardless of serum level 4, 5
• Initiate continuous telemetry until QTc normalizes 4, 5
• Obtain urgent cardiology consultation 4, 5

Mechanism of Action

Rosuvastatin reduces mature hERG protein expression on cell membranes through two pathways: (1) disrupting transport of immature hERG channels to the membrane by reducing interaction with heat shock protein 70, and (2) increasing degradation of mature hERG channels via lysosomes and proteasomes. 3 It also activates the unfolded protein response pathway through ATF6. 3 Additionally, rosuvastatin accelerates hERG channel inactivation and affects sodium and calcium channels, collectively prolonging action potential duration. 2, 3

Key Pitfalls to Avoid

• Do not assume all statins have equivalent QTc effects—atorvastatin does not prolong QTc 1, 2
• Do not ignore polypharmacy risk—even modest individual QT effects become problematic when multiple agents are combined 6, 4, 1
• Do not use Bazett's formula at heart rates >80 bpm—it overestimates QTc; use Fridericia's formula instead 4, 5
• Do not rely solely on automated ECG QTc values—manual verification is essential 4, 5