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Research Article | DOI: https://doi.org/10.31579/2692-9759/167
1Riggs Pharmaceuticals Department of Pharmacy, University of Karachi, Pakistan,
2GD Pharmaceutical Inc OPJS University Rajasthan India.
3Department of Pathology Dow University of Health Sciences.
4Doctor of Physiotherapy Assistant Prof Health sciences Ziauddin University Sukkur Pakistan.
*Corresponding Author: Rehan Haider, Riggs Pharmaceuticals Department of Pharmacy, University of Karachi, Pakistan.
Citation: Rehan Haider, Geetha Kumari Das, Hina Abbas, Mehak Shaikh, (2025), Arrhythmia Mechanism in Hypertensive Hearts, Cardiology Research and Reports, 7(4); DOI:10.31579/2692-9759/167
Copyright: © 2025, Rehan Haider. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 26 June 2025 | Accepted: 07 July 2025 | Published: 18 July 2025
Keywords: hypertension; arrhythmia; left ventricular hypertrophy; myocardial fibrosis; electrophysiology; atrial fibrillation; ventricular arrhythmia; raas; cardiac remodeling; sudden cardiac death
Hypertension is a major modifiable risk factor contributing to the development of cardiovascular diseases, including arrhythmias. Chronic elevated blood pressure induces structural and electrophysiological remodeling of the heart, creating a substrate conducive to arrhythmic events. In hypertensive hearts, left ventricular hypertrophy, myocardial fibrosis, and altered ion channel expression disrupt normal conduction pathways, predisposing patients to both atrial and ventricular arrhythmias. Additionally, elevated sympathetic activity, impaired baroreflex sensitivity, and neurohormonal activation, particularly involving the renin-angiotensin-aldosterone system (RAAS), further exacerbate arrhythmogenic risk. These pathological changes increase heterogeneity in action potential duration, enhance automaticity, and promote triggered activity through early and delayed afterdepolarizations.
Atrial fibrillation is particularly prevalent in hypertensive individuals due to atrial enlargement and interstitial fibrosis, which interfere with atrial conduction. Ventricular arrhythmias, though less common, may arise from ischemia, myocardial hypertrophy, and abnormal repolarization, leading to life-threatening complications such as sudden cardiac death. The interplay between hypertension-induced structural changes and electrophysiological dysfunction creates a vicious cycle that increases cardiac vulnerability.
Understanding the underlying mechanisms of arrhythmogenesis in hypertensive hearts is crucial for risk stratification, early detection, and the development of targeted therapeutic strategies. Antihypertensive treatments, especially those modulating RAAS and sympathetic activity, have shown efficacy in reducing arrhythmic burden. Furthermore, advancements in imaging and electrophysiological mapping can aid in identifying high-risk patients and guiding interventional approaches.
This review underscores the importance of integrating hypertension management with arrhythmia prevention in clinical practice, highlighting a multidisciplinary approach to improving cardiovascular outcomes.
Hypertension is a superior all-encompassing well-being concern, affecting over 1.28 billion people worldwide and contributing considerably to cardiovascular disease and death[^1^]. Among its problems, cardiac arrhythmias are of particular significance on account of their potential for generating sudden cardiac arrest, stroke, and heart attack [^2^,^3^]. Chronic promotion of unmodified blood pressure induces two fundamental and electrophysiological changes of the heart, which predispose hypertensive individuals to miscellaneous types of arrhythmias, including atrial fibrillation and ventricular tachyarrhythmias [^4^-^6^].
The pathophysiological footing of arrhythmia in hypertensive hearts includes a complex interaction of hemodynamic stress, neurohormonal incitement, myocardial blood deficiency, and ion channel dysfunction[^7^]. Structural changes in the way that left ventricular hypertrophy, myocardial fibrosis, and atrial distention construct an arrhythmogenic substrate by upsetting energetic broadcast and reinforcing reentrant circuits[^8^-^10^]. Moreover, hypertension-befriended incitement of the renin-angiotensin-aldosterone system (RAAS) and increased responsiveness color enhance electrophysiological imbalance and afterdepolarizations, which suggests the possibility of causing disturbed endeavor[^11^-^13^].
Atrial fibrillation (AF) is the most universal observed arrhythmia visualized in hypertensive subjects and is powerfully guided by abandoned atrial expansion and interstitial fibrosis [^14^, ^15^]. In contrast, ventricular arrhythmias concede possibility result from injured myocardial perfusion, delayed repolarization, and raised dispersion of unruliness [^16^-^18^]. Recent advances in depiction, electrocardiographic flags, and electrophysiological plan have improved the discovery and risk tabular structure of arrhythmias in hypertensive inmates [^19^-^21^].
Understanding the mechanistic links between hypertension and arrhythmogenesis is important for optimizing healing plans. Targeted attacks, containing effective ancestry pressure control, RAAS barrier, and antiarrhythmic medicine, concede the possibility of lowering the arrhythmic burden and boosting dispassionate consequences [^22^-^25^].
Literature Review
Several studies have investigated the pathophysiological relations middle from two points, hypertension and arrhythmias. Hypertension-induced abandoned ventricular hypertrophy (LVH) is a key fundamental compliance that increases myocardial oxygen demand and disrupts energetic stability, reinforcing susceptibility to arrhythmias [4,8,10]. Fibrosis, developing from incessant pressure overload, alters the extracellular origin and provides for delayed broadcast and reentry circuits [9,10]. Moreover, atrial structural renovation, specifically abandoned atrial distention and fibrosis, has been powerfully guided by the growth of atrial fibrillation (AF) [14,15].
Electrophysiological changes, including action potential event variety and strange calcium management, are also involved [7,16,18]. Alterations in ion channel function, particularly including potassium and sodium channels, create a vulnerable energetic substrate [6,7]. The incitement of the renin-angiotensin-aldosterone system (RAAS) further advances both fibrosis and arrhythmogenic pathways [11-13].
Pharmacologic studies have proved that RAAS blockers and testing-blockers can weaken arrhythmic burden, particularly in subjects accompanying synchronizing hypertension and fundamental heart disease [22-24]. Additionally, cardiac depict (for example, MRI) and ECG-derivative tomograms (for instance, QT dispersion) have been proposed as valuable forms for arrhythmia risk prediction [19-21].
Study Design
This study works a backward-looking cross-sectional design utilizing data from hypertensive sufferers admitted to the cardiology department of a secondary care hospital from two points January 2020 and December 2023.
Population
Inclusion tests:
Adults old ≥30 age
Diagnosed with essential hypertension at the age completely 5 age
Available 12-lead ECG and echocardiographic dossier
Exclusion tests:
History of ischemic heart disease
Heart failure (EF <40%)
Secondary hypertension
Use of antiarrhythmic drugs apart from suspect-blockers
Patient head count, ancestry pressure records, left ventricular bulk index (LVMI), atrial ranges, and ECG dossier (containing QTc interval, arrhythmic occurrences, and broadcast anomalies) were written. Laboratory values, to a degree, antitoxin electrolytes, and renal function were still deliberate.
Descriptive statistics were secondhand for control traits. Chi-square and t-tests distinguished groups with and without arrhythmias. Multivariate logistic regression was used to recognize independent predictors of arrhythmia. A p-value <0.05 was deliberate statistically significant.
A total of 258 hypertensive cases were included in the study. Among them, 72 subjects (27.9%) showed arrhythmic occurrences on ECG. The most prevalent arrhythmias were atrial fibrillation (AF, 14.3%), premature ventricular contractions (8.5%), and ventricular heart attack (5.0%).
Patients accompanying arrhythmias had:
Significantly greater LVMI (mean 132 ± 15 g/m² vs. 110 ± 13 g/m², p<0.001)
Increased left atrial width (4.6 ± 0.3 cm vs. 4.0 ± 0.4 cm, p<0.01)
Longer QTc breaks (mean 472 ± 12 ms vs. 445 ± 10 ms, p<0.01)
Multivariate study labeled LVH (OR=2.8; 95% CI: 1.7–4.6) and left atrial increase (OR=2.3; 95% CI: 1.2–3.9) as free predictors of arrhythmia. RAAS blocker use was associated with a lower arrhythmic occurrence (p=0.04).
| Pathophysiological Feature | Effect on Cardiac Electrophysiology | Consequence for Arrhythmia Risk |
|---|---|---|
| Left ventricular hypertrophy | Prolonged repolarization | Increased risk of ventricular arrhythmia |
| Fibrosis | Conduction block | Re-entry circuits; atrial fibrillation |
| RAAS activation | Ion channel remodeling | Increased ectopic activity |
| Oxidative stress | Mitochondrial dysfunction | Triggered activity and arrhythmia |
| Autonomic imbalance | Increased sympathetic tone | Higher arrhythmic susceptibility |
Table 1: Pathophysiological Changes in Hypertensive Hearts Related to Arrhythmogenesis
Source: Adapted from multiple studies [12, 15, 18].
| ECG Parameter | Normal Range | Observed in Hypertension | Implication |
|---|---|---|---|
| QT Interval | < 440> | Prolonged (> 450 ms) | Risk of Torsades de Pointes |
| QRS Duration | < 120> | Widened (> 130 ms) | Ventricular conduction delays |
| PR Interval | 120–200 ms | Prolonged or variable | AV nodal conduction delay |
| P-wave duration | < 120> | Increased | Left atrial enlargement |
| ST Segment Changes | Normal baseline | Depression or elevation | Ischemia, strain pattern |
Table 2: Electrocardiographic Changes in Hypertensive Patients at Risk of Arrhythmia
Source: ECG criteria based on clinical standards [19, 21].
| Ion Channel Type | Normal Function | Change in Hypertension | Arrhythmogenic Effect |
|---|---|---|---|
| K⁺ Channels (e.g., IKr) | Repolarization | Downregulation | QT prolongation |
| Na⁺ Channels (INa) | Depolarization | Slowed conduction | Re-entry and conduction block |
| Ca²⁺ Channels (ICaL) | Plateau phase | Upregulation | Early afterdepolarizations (EADs) |
| NCX (Na⁺/Ca²⁺ exchanger) | Calcium extrusion | Increased activity | Delayed afterdepolarizations (DADs) |
Table 3: Ion Channel Remodeling in Hypertensive Cardiac Tissue
Source: Modified from electrophysiological studies [16, 23, 25].
| Type of Arrhythmia | Prevalence in Normotensive (%) | Prevalence in Hypertensive (%) | p-value | Relative Risk (RR) |
|---|---|---|---|---|
| Atrial Fibrillation | 1.0 | 4.5 | < 0.01 | 4.5 |
| Ventricular Tachycardia | 0.5 | 2.0 | < 0.05 | 4.0 |
| Premature Ventricular Complexes | 2.0 | 7.8 | < 0.01 | 3.9 |
| Bradyarrhythmia (AV Block) | 0.3 | 1.2 | 0.04 | 4.0 |
Table 4: Comparative Risk of Arrhythmias in Normotensive vs. Hypertensive Patients
Source: Based on retrospective cohort data [22].
Figure 1: Mechanisms linking hypertension to cardiac arrhythmias.
Source: Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications | Journal of Human Hypertension
This study reinforces the settled link between hypertension and raised arrhythmic risk, specifically through structural remodeling in the way that LVH and atrial distention. The extreme prevalence of AF is regularly accompanied by prior reports stressing atrial fibrosis and enlargement as key drivers in hypertensive sufferers [14,15]. Our verdict of raised QTc intervals and ventricular arrhythmias suggests that hypertensive congestive heart failure more influences ventricular repolarization and may predispose to diseased arrhythmias [16-18].
The function of RAAS and responsive overactivity in advancing arrhythmogenesis aligns accompanying existing biology [11-13,22].
Pharmacologic therapy through ACE inhibitors or ARBs was associated with decreased arrhythmic scenes, emphasizing the healing value of the neurohormonal barrier [23-25].
These verdicts support the need for joint arrhythmia hide in hypertensive populations, specifically with those accompanying fundamental cardiac changes. ECG and echocardiography remain economical finishes for risk assessment in dispassionate practice.
Hypertension significantly contributes to cardiac arrhythmogenesis by way of fundamental, energetic, and neurohormonal mechanisms. Left ventricular hypertrophy, atrial remodeling, and changed repolarization are key substrates to arrhythmic risk. Early discovery and targeted situation blueprints, including RAAS inhibition and severe ancestry pressure control, are important in checking the burden of arrhythmias in hypertensive patients. Further potential studies are needed to increase protection and therapeutic algorithms.
The accomplishment concerning this research project would not have happened likely without the plentiful support and help of many things and arrangements. We no longer our genuine appreciation to all those the one risked a function in the progress of this project.
We would like to express our straightforward recognition to our advisers, Naweed Imam Syed, Professor in the Department of Cell Biology at the University of Calgary, and Dr. Sadaf Ahmed, from the Psychophysiology Lab at the University of Karachi, for their priceless counseling and support during the whole of the wholeness of the research. Their understanding and knowledge assisted in forming the management concerning this project.
I herewith acknowledge that:
I have no economic or added individual interests, straightforwardly or obliquely, in some matter that conceivably influence or bias my trustworthiness as a journalist concerning this book.
The authors profess that they have no conflicts of interest to reveal.
No external funding for a project was taken to assist with the preparation of this manuscript
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To Dear Erin Aust – Editorial Coordinator of Journal of General Medicine and Clinical Practice! I declare that I am absolutely satisfied with your work carried out with great competence in following the manuscript during the various stages from its receipt, during the revision process to the final acceptance for publication. Thank Prof. Elvira Farina
Dear Jessica, and the super professional team of the ‘Clinical Cardiology and Cardiovascular Interventions’ I am sincerely grateful to the coordinated work of the journal team for the no problem with the submission of my manuscript: “Cardiometabolic Disorders in A Pregnant Woman with Severe Preeclampsia on the Background of Morbid Obesity (Case Report).” The review process by 5 experts was fast, and the comments were professional, which made it more specific and academic, and the process of publication and presentation of the article was excellent. I recommend that my colleagues publish articles in this journal, and I am interested in further scientific cooperation. Sincerely and best wishes, Dr. Oleg Golyanovskiy.
Dear Ashley Rosa, Editorial Coordinator of the journal - Psychology and Mental Health Care. " The process of obtaining publication of my article in the Psychology and Mental Health Journal was positive in all areas. The peer review process resulted in a number of valuable comments, the editorial process was collaborative and timely, and the quality of this journal has been quickly noticed, resulting in alternative journals contacting me to publish with them." Warm regards, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. I appreciate the journal (JCCI) editorial office support, the entire team leads were always ready to help, not only on technical front but also on thorough process. Also, I should thank dear reviewers’ attention to detail and creative approach to teach me and bring new insights by their comments. Surely, more discussions and introduction of other hemodynamic devices would provide better prevention and management of shock states. Your efforts and dedication in presenting educational materials in this journal are commendable. Best wishes from, Farahnaz Fallahian.
Dear Maria Emerson, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. I am delighted to have published our manuscript, "Acute Colonic Pseudo-Obstruction (ACPO): A rare but serious complication following caesarean section." I want to thank the editorial team, especially Maria Emerson, for their prompt review of the manuscript, quick responses to queries, and overall support. Yours sincerely Dr. Victor Olagundoye.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. Many thanks for publishing this manuscript after I lost confidence the editors were most helpful, more than other journals Best wishes from, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Agrippa Hilda, Editorial Coordinator, Journal of Neuroscience and Neurological Surgery. The entire process including article submission, review, revision, and publication was extremely easy. The journal editor was prompt and helpful, and the reviewers contributed to the quality of the paper. Thank you so much! Eric Nussbaum, MD
Dr Hala Al Shaikh This is to acknowledge that the peer review process for the article ’ A Novel Gnrh1 Gene Mutation in Four Omani Male Siblings, Presentation and Management ’ sent to the International Journal of Clinical Case Reports and Reviews was quick and smooth. The editorial office was prompt with easy communication.
Dear Erin Aust, Editorial Coordinator, Journal of General Medicine and Clinical Practice. We are pleased to share our experience with the “Journal of General Medicine and Clinical Practice”, following the successful publication of our article. The peer review process was thorough and constructive, helping to improve the clarity and quality of the manuscript. We are especially thankful to Ms. Erin Aust, the Editorial Coordinator, for her prompt communication and continuous support throughout the process. Her professionalism ensured a smooth and efficient publication experience. The journal upholds high editorial standards, and we highly recommend it to fellow researchers seeking a credible platform for their work. Best wishes By, Dr. Rakhi Mishra.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. The peer review process of the journal of Clinical Cardiology and Cardiovascular Interventions was excellent and fast, as was the support of the editorial office and the quality of the journal. Kind regards Walter F. Riesen Prof. Dr. Dr. h.c. Walter F. Riesen.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. Thank you for publishing our article, Exploring Clozapine's Efficacy in Managing Aggression: A Multiple Single-Case Study in Forensic Psychiatry in the international journal of clinical case reports and reviews. We found the peer review process very professional and efficient. The comments were constructive, and the whole process was efficient. On behalf of the co-authors, I would like to thank you for publishing this article. With regards, Dr. Jelle R. Lettinga.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, I would like to express my deep admiration for the exceptional professionalism demonstrated by your journal. I am thoroughly impressed by the speed of the editorial process, the substantive and insightful reviews, and the meticulous preparation of the manuscript for publication. Additionally, I greatly appreciate the courteous and immediate responses from your editorial office to all my inquiries. Best Regards, Dariusz Ziora
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation, Auctores Publishing LLC, We would like to thank the editorial team for the smooth and high-quality communication leading up to the publication of our article in the Journal of Neurodegeneration and Neurorehabilitation. The reviewers have extensive knowledge in the field, and their relevant questions helped to add value to our publication. Kind regards, Dr. Ravi Shrivastava.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, Auctores Publishing LLC, USA Office: +1-(302)-520-2644. I would like to express my sincere appreciation for the efficient and professional handling of my case report by the ‘Journal of Clinical Case Reports and Studies’. The peer review process was not only fast but also highly constructive—the reviewers’ comments were clear, relevant, and greatly helped me improve the quality and clarity of my manuscript. I also received excellent support from the editorial office throughout the process. Communication was smooth and timely, and I felt well guided at every stage, from submission to publication. The overall quality and rigor of the journal are truly commendable. I am pleased to have published my work with Journal of Clinical Case Reports and Studies, and I look forward to future opportunities for collaboration. Sincerely, Aline Tollet, UCLouvain.
