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Learn more: PMC Disclaimer | PMC Copyright Notice Eur Heart J Case Rep . 2026 Mar 18;10(4):ytag219. doi: 10.1093/ehjcr/ytag219 Search in PMC Search in PubMed View in NLM Catalog Add to search Efficacy of ranolazine in reducing complex premature ventricular contractions in a patient with mitral valve prolapse: a case report Nicola Tarantino Nicola Tarantino 1 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 2 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA Conceptualization, Data curation, Supervision, Writing - original draft, Writing - review & editing Find articles by Nicola Tarantino 1, 2, ✉, 3, # , Kaiyu Tio Kaiyu Tio 3 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA Writing - original draft, Writing - review & editing Find articles by Kaiyu Tio 3, # , Aldo Schenone Aldo Schenone 4 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 5 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA Data curation Find articles by Aldo Schenone 4, 5 , Luigi Di Biase Luigi Di Biase 6 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 7 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA Supervision, Validation Find articles by Luigi Di Biase 6, 7 Editors: Panteleimon E Papakonstantinou , Nikesh Jathanna , Michael Spartalis , Ugur Canpolat , Deepti Ranganathan Author information Article notes Copyright and License information 1 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 2 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA 3 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 4 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 5 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA 6 Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 7 Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA ✉ Corresponding author. Tel: +1 (718) 920 4889, Email: [email protected] # Nicola Tarantino and Kaiyu Tio contributed equally to the study. 3 Conflict of interest . The authors declare that they have no conflicts of interest relevant to the content of this article. Roles Nicola Tarantino : Conceptualization, Data curation, Supervision, Writing - original draft, Writing - review & editing Kaiyu Tio : Writing - original draft, Writing - review & editing Aldo Schenone : Data curation Luigi Di Biase : Supervision, Validation Panteleimon E Papakonstantinou : Handling Editor Nikesh Jathanna : Editor Michael Spartalis : Editor Ugur Canpolat : Editor Deepti Ranganathan : Editor Received 2025 Sep 26; Revised 2026 Jan 14; Accepted 2026 Mar 13; Collection date 2026 Apr. © The Author(s) 2026. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License ( https://creativecommons.org/licenses/by-nc/4.0/ ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact [email protected]. PMC Copyright notice PMCID: PMC13070374 PMID: 41978766 Abstract Background Pharmacological options for treating arrhythmic mitral valve prolapse (aMVP) are limited and anecdotal. Ranolazine as an antiarrhythmic has yielded satisfactory outcomes in suppressing ventricular arrhythmias, but its role in the case of aMVP is unknown. Case summary A 62-year-old female presented complaining of palpitations. ECG and the cardiac monitor showed very frequent and complex monomorphic premature ventricular contractions (PVCs), likely from the posteromedial papillary muscle. Cardiac MRI revealed the presence of mitral valve prolapse. Empirical treatment with ranolazine 1000 mg b.i.d. was initiated for antiarrhythmic purposes, with subjective clinical improvement and objective reduction of complex PVCs after 32 months of follow-up. Discussion Papillary muscle PVCs are a common finding in patients with aMVP. Antiarrhythmic properties of ranolazine can be safely used in patients with contraindications to other interventions for the treatment of PVCs associated with mitral valve prolapse. The effect seems more evident on complex PVCs and ventricular tachycardia and can be attributed to an intrinsic use dependence of the drug; therefore, this treatment should be explored for selected cases. To the best of our knowledge, this is the first report of a case of improvement in PVCs following the administration of a high dose of ranolazine in a patient with aMVP. Future investigations on a larger scale should focus on whether ranolazine can be safely used as an alternative treatment to reduce the risks of ventricular arrhythmia and improve patients’ prognosis. Keywords: Antiarrhythmic, Case report, Mitral valve prolapse, Papillary muscle, Premature ventricular complex, Ranolazine Learning points. Papillary muscle PVCs are common in aMVP due to mechanical tension on the subvalvular apparatus and myxomatous changes. By inhibiting the late phase of the sodium current with a use-dependent effect, ranolazine might effectively reduce complex PVCS also in aMVP cases. Further studies are needed to confirm and explore the mechanisms underlying this finding. Introduction Arrhythmic mitral valve prolapse (aMVP) is a valvular disorder characterized by systolic protrusion of the mitral leaflets into the left atrium, associated with ventricular arrhythmias and, rarely, sudden cardiac death. 1 The recent European Heart Rhythm expert consensus advocates catheter ablation or selective antiarrhythmics as management options for this specific population. 2 Ranolazine, an antianginal medication that inhibits the late phase of sodium influx (late INa + ), has been anecdotally used in cases of isolated premature ventricular contractions (PVCs), and, in a multicentre randomized controlled trial, it proved its safety and partial efficacy compared to placebo in patients with implantable defibrillators. 3 , 4 Nonetheless, its use as an antiarrhythmic is still off-label. Summary figure Visual summary—timeline of the case First visit A 62-year-old female complains of palpitations. ECG shows frequent monomorphic PVCs, likely originating from the posteromedial papillary muscle. The previous echocardiogram showed moderate mitral regurgitation with normal LVEF. 4-month follow-up The extended cardiac monitoring reveals a total PVC burden of 47%. The patient does not tolerate mexiletine and starts empiric therapy with ranolazine 500 mg b.i.d. 6-month follow-up cMRI confirms the presence of MVP with moderate regurgitation and reduced LVEF, and the second cardiac monitor shows unchanged PVC burden. The patient refuses catheter ablation, and ranolazine is increased to 1000 mg b.i.d. 7-month follow-up A third cardiac monitor indicates a substantially reduced burden of PVCs (36%), mainly represented by a decrease in complex PVCs (<1% from 31.2%). The patient is asymptomatic, tolerating ranolazine well. 12-month follow-up A new echocardiogram shows recovery of the LVEF and reduction of the mitral regurgitation. The patient remains asymptomatic, and serial ECGs do not reveal any clinical PVCs. 25-month follow-up The patient remains asymptomatic, and the burden of PVCs on the cardiac monitor is <1%. She decides to remain on pharmacological treatment. 32-month follow-up After 26 months of therapy with maximal dose of ranolazine, the patient has experienced no events and remains asymptomatic. Open in a new tab Case presentation A 62-year-old woman with a history of hypertension, hyperlipidaemia, obesity (BMI 38), and non-obstructive coronary artery disease presented for evaluation of palpitations. A baseline echocardiogram from 1 year prior revealed a preserved left ventricular ejection fraction (LVEF, 68%) and moderate mitral regurgitation. She denied chest pain, dyspnoea, syncope, and heart failure symptoms, and she had no family history of myocardial infarction, sudden cardiac death, or inherited cardiomyopathy. The 12-lead ECG obtained at the present visit showed frequent monomorphic PVCs in singlets, couplets, and triplets featuring a posteromedial papillary muscle (right bundle branch block-like, superior axis; RR in V1; R/S ratio <1 in V6). This abnormality was not seen on her previous ECG from 5 years prior ( Figures 1A–C ). The patient was euvolemic, and the physical examination was unremarkable apart from an irregular rhythm consistent with PVCs and a 3/6 telesystolic murmur at the apical focus. Figure 1. Open in a new tab (A) Patient’s ECG dated 2017. ( B, C ) Twelve-lead ECG in 2022, showing frequent right-bundle-inferior axis PVCs, in singlets, couplets, and triplets (C) . ( D) ECG in 2024 after 15 months of therapy with ranolazine 1000 mg b.i.d. A 14-day extended cardiac monitor revealed a 47% PVC daily burden, predominantly represented by couplets with a balanced circadian distribution, and the fastest run of five beats at 154 b.p.m., corresponding with the patient’s triggered event ( Figure 2A ). Given her grossly normal recent echocardiogram, her insurance approved advanced imaging with cardiac MRI (CMRI), which was ordered to rule out the presence of structural cardiomyopathy. To suppress PVCs and improve symptoms, with additional intent to optimize the upcoming imaging, mexiletine 150 mg t.i.d. and a low dose of metoprolol tartrate (50 mg b.i.d., because of her episodic marked bradycardia—39 b.p.m.—on the monitor) were prescribed. However, the patient stopped taking mexiletine due to intense dizziness. Dose escalation of metoprolol and use of non-dihydropyridine calcium channel blockers were avoided in the first place due to bradycardia previously noted on monitoring. In the absence of contemporaneous assessment of LV function, pending CMRI, flecainide was avoided. Class III antiarrhythmics were also avoided due to the patient’s concern of side effects based on her experience with mexiletine. Empiric treatment with ranolazine was offered due to its safety profile and promising reports of early experiences. After comparing it with amiodarone and sotalol, the patient decided on treatment with ranolazine, starting at 500 mg b.i.d. Figure 2. Open in a new tab (A) The fastest non-sustained VT before (top) and after initiation of ranolazine 1000 mg (bottom). (B) Breakdown of the ectopic beats burden from the 14-day cardiac monitors before (left) and after 1 month of treatment with ranolazine 1000 mg. (C) Overall heart rate (top), QTc analysis (middle), and ectopic beats daily burden (bottom) after 25 months of treatment with the full dose of ranolazine on her 5-day cardiac monitor. At the 6-month follow-up, the repeated 14-day cardiac monitor showed an unchanged burden. Therefore, the ranolazine dose was doubled. CMRI revealed low-normal LVEF (52%) with segmental hypokinesis and linear subendocardial late gadolinium enhancement (LGE) involving the mid to apical inferior wall near the insertion of the inferomedial papillary muscle, with the presence of anterior mitral leaflet prolapse (A2/A3 scallops) and moderate mitral regurgitation ( Figure 3 and video in Supplementary material ). The severity of the mitral valve insufficiency was consistent with what was observed on her prior echocardiogram. No other MVP features were noted. The differential diagnosis included prior myocardial infarction along the distal posterolateral ventricular branch/obtuse marginal branch territory versus fibrosis at the papillary muscle insertion site in association with mitral valve prolapse. Since the patient had a coronary angiography negative for coronary artery disease, and did not report any symptoms suggestive of ischaemia, the findings were most likely suggestive of aMVP with initial PVC-mediated cardiomyopathy. BNP was ordered as part of the diagnostic evaluation of heart failure with preserved ejection fraction; however, it could not be performed due to the temporary unavailability of laboratory reagents. The patient initiated guideline-directed therapy for heart failure but refused catheter ablation as the first line for rhythm control and treatment of her secondary cardiomyopathy. After re-examining the currently suggested pharmacological options, which included amiodarone and sotalol, she agreed to continue with 1000 mg b.i.d. of ranolazine. Metoprolol tartrate was switched to metoprolol succinate 100 mg o.d. for dosing convenience and titration of the beta-blockade. The addition of gliflozins as part of the treatment of her heart failure with preserved ejection fraction was recommended; however, in the shared decision-making process, the patient declined due to potential non-compliance. Figure 3. Open in a new tab (A) Anterior MV prolapse (A2/A3 scallops). (B) Linear subendocardial LGE involving the mid to apical inferior walls near the insertion of the inferomedial papillary muscle. Note the basal inferior wall crypts (two arrows). One month later, the repeated extended 14-day cardiac monitor showed a reduction in the overall daily PVC burden from 47 862/day (47% burden) to 32 881/day (36%) and substantial suppression of couplets and triplets, with combined couplets and triplets count decreasing from 15 434/day to 391/day, equivalent to a 97% absolute reduction and correlating with symptom improvement. Of note, there was a parallel relative doubling in the proportion of singlets from 16 037/day to 32 030/day. The runs of non-sustained ventricular tachycardias (NSVT) diminished from 118/day to <2/day ( Figure 2B ). A repeated 12-lead ECG showed normal QTc (440 ms compared to 414 ms at her baseline, calculated according to Bazett’s formula) and no PVCs ( Figure 1A and D ). Additionally, the LVEF normalized on her repeated echocardiogram (65%) with qualitatively reduced mitral regurgitation, reclassified as mild, compared with the baseline echocardiogram (see video in Supplementary material ). Experiencing decreased PVC burden and minimal palpitations, she deferred radiofrequency catheter ablation and continued with her current treatment plan. Her 5-day cardiac monitor at 25 months showed 481 PVC/day (<1% burden, Figure 2C ). After 32 months of follow-up, the patient has not experienced any significant cardiac events and remains mainly asymptomatic, with no PVCs and with a QTc of 416 ms on the 12-lead ECG ( Table 1 , Figure 4 ). Table 1. QT intervals since initiation of ranolazine Time (months) HR (b.p.m.) QT/QTc with Bazett (ms) Baseline 56 446/414 1 51 440/424 a 4 52 454/423 a 7 46 502/440 b 12 46 471/412 19 55 472/452 25 54 c 450/423 c 32 51 452/416 Open in a new tab b.p.m., beats per minute; HR, heart rate; ms, milliseconds. a Using ranolazine 500 mg b.i.d. b After 1 month of ranolazine 1000 mg bid. c Indicates average values from the cardiac monitor. Figure 4. Open in a new tab Patient’s ECG at 32 months (26 months in therapy with ranolazine 1000 mg b.i.d.). Discussion Frequent monomorphic PVCs are observed in half of the patients with MVP, and according to a single-centre observational study, MVP-related PVCs account for 4% of PVC cases requiring ablation. 5 Female patients with MVP are more commonly affected by PVCs, which typically originate from the posterior papillary muscle in over half of the patients. Ventricular fibrillation at presentation has been reported in 16% of these cases (4 out of 25 with aMVP). 5 The unique pathophysiological interplay between MVP and PVCs is explained by the abnormal systolic displacement of the mitral leaflets, leading to excessive mechanical stretching of the papillary muscles and priming myocytes for triggered activity. 6 The continuous tension on the subvalvular apparatus also causes fibrotic changes responsible for re-entry. 1 Ranolazine is a piperazine derivative that inhibits late INa + , resulting in shorter action potentials and decreased intracellular sodium accumulation, which indirectly reduces calcium load via the sodium-calcium exchanger. 7 The combined effect of these changes lowers the likelihood of abnormal depolarizations and PVCs. Based on the serendipitous evidence that ranolazine reduced NSVT in the MERLIN TIMI 36 trial, 8 Nanda et al . 9 first reported that the 1 g b.i.d. of ranolazine suppressed PVCs from 36% to 2% and ventricular tachycardia in a patient with ischaemic cardiomyopathy and severely reduced ejection fraction. Murray subsequently noted a more substantial reduction in complex PVCs (a reduction of >90% in couplets and runs) than in isolated PVCs in more than two-thirds of the 59 patients. 10 This finding is in line with our clinical observation of a parallel significant increment of ventricular singlets compared to an even more substantial reduction (−97%) of couplets and triplets. Based on its use-dependent effect demonstrated in vitro , we can only speculate that ranolazine has a more prominent effect on complex PVC and that an electrical remodelling occurs as the number of couplets and runs diminishes. 11 Furthermore, its attenuation of stretch-induced ventricular fibrillation and the presence in the papillary muscle of Purkinje cells, which are primarily rate-dependent on late INa + , could explain this possible selectivity of ranolazine as an antiarrhythmic for premature contractions originating from the subvalvular apparatus. 12 , 13 , 14 The current consensus on the treatment of aMVP recommends PVC ablation in symptomatic patients with decreased LV function, 2 being acutely successful in 76% of cases. 5 Beta-blockers, dihydropyridine calcium blockers, Ic antiarrhythmics, sotalol, and amiodarone are considered reasonable options, 1 with anecdotal success using dronedarone and mexiletine reported as well; 5 however, improvement in LV function varies with each agent. In the case presented here, the patient refused invasive treatment; her compromised LV function limited the use of Ic drugs, and after experiencing side effects from mexiletine, she was highly concerned about Class III agents. Therefore, after ascertaining the low-risk phenotype given the absence of (i) mitral annular disjunction, (ii) negative T waves in inferior leads, and (iii) rapid non-sustained VT, the shared decision was to continue with pharmacological management, so ranolazine was introduced as an off-label option, motivated by early experiences. 3 , 4 , 9 , 10 Ranolazine has been associated with reductions in PVC burden and is generally well-tolerated. Side effects, mainly dizziness and constipation, are reported in 6%–14% of the treated subjects, 3 , 10 and despite its effects on the IKr channel, no relevant QT prolongation has been reported when used as a single antiarrhythmic agent. 15 Although this case demonstrates PVC suppression in aMVP following initiation of ranolazine, the ability to establish a distinct or generalizable role for this drug remains limited without further support beyond a single case. The observed improvement in LVEF and reduction in mitral regurgitation may be multifactorial and cannot be attributed solely to ranolazine. Finally, we acknowledge that ablation might have been more effective; however, for patients unwilling to undergo invasive procedures and at low arrhythmic risk, symptom control and LVEF recovery are sufficient. For these patients, ranolazine may serve as an alternative with a favourable long-term safety profile; however, its role in this population requires further study. Supplementary Material ytag219_Supplementary_Data ytag219_supplementary_data.zip (10.8MB, zip) Acknowledgements The authors thank Irma Serrano, LPN, for providing part of the medical records. Contributor Information Nicola Tarantino, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA; Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA. Kaiyu Tio, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA. Aldo Schenone, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA; Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA. Luigi Di Biase, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA; Montefiore Medical Center, University Hospital at Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA. Lead author biography Dr Nicola Tarantino received his MD degree from the University of Bari (Bari, Italy) in 2012. Since 2021, he has been working as a cardiologist and electrophysiologist at Montefiore Medical Center in New York City (USA). His areas of medical interest include pacing devices, lead extractions, the prevention of sudden cardiac death, cardiac ablations, and cardiac pharmacology for the treatment of arrhythmias. Supplementary material Supplementary material is available at European Heart Journal – Case Reports online. Author contributions Nicola Tarantino (Conceptualization, Data curation, Supervision [lead], Writing—original draft, Writing—review & editing [equal]), Kaiyu Tio (Writing—original draft, Writing—review & editing [equal]), Aldo Schenone (Data curation [supporting]), and Luigi Di Biase (Supervision, Validation [supporting]) Consent: The authors confirm that informed written consent for the submission and publication of this case report, including images and associated text, has been obtained from the patient in accordance with COPE guidance. Funding None declared. Data availability The data underlying this article cannot be shared publicly to protect the patient’s sensitive information, ensuring privacy and security for medical records. This case report is based entirely on the clinical care of a single patient with a rare disease. All relevant information is presented in the manuscript, and no additional data is available. References 1. 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Pacing Clin Electrophysiol 2011;34:1600–1606. [ DOI ] [ PubMed ] [ Google Scholar ] Associated Data This section collects any data citations, data availability statements, or supplementary materials included in this article. Supplementary Materials ytag219_Supplementary_Data ytag219_supplementary_data.zip (10.8MB, zip) Data Availability Statement The data underlying this article cannot be shared publicly to protect the patient’s sensitive information, ensuring privacy and security for medical records. This case report is based entirely on the clinical care of a single patient with a rare disease. All relevant information is presented in the manuscript, and no additional data is available. Articles from European Heart Journal. 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