The Federal Reserve's balance sheet has undergone significant changes since 2007, reflecting its response to major economic crises. From a modest *** trillion U.S. dollars at the end of 2007, it ballooned to approximately **** trillion U.S. dollars by June 2025. This dramatic expansion, particularly during the 2008 financial crisis and the COVID-19 pandemic - both of which resulted in negative annual GDP growth in the U.S. - showcases the Fed's crucial role in stabilizing the economy through expansionary monetary policies. Impact on inflation and interest rates The Fed's expansionary measures, while aimed at stimulating economic growth, have had notable effects on inflation and interest rates. Following the quantitative easing in 2020, inflation in the United States reached ***** percent in 2022, the highest since 1991. However, by *************, inflation had declined to *** percent. Concurrently, the Federal Reserve implemented a series of interest rate hikes, with the rate peaking at **** percent in ***********, before the first rate cut since ************** occurred in **************. Financial implications for the Federal Reserve The expansion of the Fed's balance sheet and subsequent interest rate hikes have had significant financial implications. In 2023, the Fed reported a negative net income of ***** billion U.S. dollars, a stark contrast to the ***** billion U.S. dollars profit in 2022. This unprecedented shift was primarily due to rapidly rising interest rates, which caused the Fed's interest expenses to soar to over *** billion U.S. dollars in 2023. Despite this, the Fed's net interest income on securities acquired through open market operations reached a record high of ****** billion U.S. dollars in the same year.

Long QT Syndrome Treatment Market size was valued at USD 1.1 Billion 2023 and is projected to reach USD 2.4 Billion by 2030, growing at a CAGR of 8.2% during the forecasted period 2024 to 2030

Global Long QT Syndrome Treatment Market Drivers

The growth and development of the Long QT Syndrome Treatment Market drivers. These factors have a big impact on how Long QT Syndrome Treatment are demanded and adopted in different sectors. Several of the major market forces are as follows:

Growing Prevalence of Long QT Syndrome: Cases of Long QT Syndrome are becoming more widely recognized globally as knowledge and diagnostic tools advance. There is a growing need for efficient management techniques and therapies due to the condition's increasing prevalence.

Improvements in Genetic Testing and Diagnosis: Thanks to technological advancements in genetic testing, Long QT Syndrome can now be diagnosed more precisely and effectively, and certain genetic abnormalities linked to the illness can be found. The need for LQTS therapy is driven by the ability to intervene and treat promptly following an early diagnosis.

Growing Emphasis on Personalized Medicine: As our knowledge of the genetic underpinnings of Long QT Syndrome has improved, so too has our focus on customized treatment plans based on the unique genetic profiles of each patient. Targeted interventions and genotype-specific medications are examples of personalized medicine tactics that could spur innovation in the treatment of long-QT syndrome.

Increasing Awareness and Education Initiatives: Governmental organizations, patient advocacy groups, and healthcare organizations have stepped up their awareness campaigns, educational initiatives, and advocacy work to help identify, diagnose, and treat Long QT Syndrome early on. Demand for LQTS treatments is driven by increased awareness among the general public and healthcare professionals.

Technical Developments in Treatment Modalities: Long QT Syndrome treatment choices have become increasingly effective as a result of technological advancements in cardiac electrophysiology, implantable devices, and medication. Technological developments like implantable cardioverter-defibrillators (ICDs), cardiac pacing, and innovative medication therapy enhance patient outcomes and increase the market for LQTS treatments.

Long QT Syndrome Treatment Market Outlook

The global market size for Long QT Syndrome Treatment was valued at USD 2.1 billion in 2023 and is projected to reach approximately USD 4.5 billion by 2032, growing at a compound annual growth rate (CAGR) of 9.3% during the forecast period. One of the significant growth factors driving this market is the increasing prevalence of cardiac disorders coupled with advancements in medical technology.

The growth of the Long QT Syndrome Treatment market can be attributed to the rising incidence of cardiovascular diseases globally. According to the World Health Organization, cardiovascular diseases are the leading cause of death worldwide, prompting healthcare providers to seek more efficient and effective treatment methodologies. Furthermore, the aging global population is more prone to such conditions, thereby increasing the demand for Long QT Syndrome treatments. Enhanced awareness and screening programs have also played a crucial role in early diagnosis and subsequent treatment of the syndrome, fueling market growth.

Technological advancements in the healthcare sector have significantly impacted the Long QT Syndrome Treatment market. The development of sophisticated medical devices like Implantable Cardioverter Defibrillators (ICDs) and automated external defibrillators (AEDs) has revolutionized the way cardiac conditions are treated. Moreover, advancements in pharmacogenomics and personalized medicine have opened new avenues for tailored treatment options, making therapies more effective and safer for patients. Investments in research and development by pharmaceutical companies and medical device manufacturers have also contributed to the market's expansion.

Regulatory support and favorable reimbursement policies in developed countries have further boosted the market growth. Governments in regions such as North America and Europe have implemented supportive healthcare policies and funding, which facilitate easier access to advanced treatments. Additionally, increasing healthcare expenditure and the rise of private healthcare providers in emerging economies have also contributed to market growth. These regions are witnessing a significant rise in the adoption of advanced medical technologies, supported by growing disposable incomes and better healthcare infrastructure.

The regional outlook for the Long QT Syndrome Treatment market shows significant growth potential across various regions. North America currently holds the largest market share, driven by high healthcare expenditure, robust infrastructure, and a higher prevalence of cardiovascular diseases. Europe follows closely, supported by strong healthcare systems and increased research activities. The Asia Pacific region is expected to witness the highest growth rate due to rising healthcare awareness, increased government spending on healthcare facilities, and a growing patient pool. Latin America and the Middle East & Africa are also experiencing gradual market growth, primarily due to improving healthcare infrastructure and increasing awareness about the syndrome and its treatments.

Beta Blockers Analysis

Beta blockers are one of the most commonly prescribed treatments for Long QT Syndrome. These medications work by blocking the effects of adrenaline on the heart, thereby reducing the heart rate and decreasing the likelihood of arrhythmias. The use of beta blockers has proven to be highly effective in managing symptoms of Long QT Syndrome, particularly in preventing sudden cardiac events. The market for beta blockers in the treatment of Long QT Syndrome is driven by their established efficacy, wide availability, and relatively low cost compared to other treatment modalities.

One of the critical factors contributing to the growth of the beta blockers segment is the strong clinical evidence supporting their use. Numerous studies have demonstrated the efficacy of beta blockers in reducing the risk of cardiac events in patients with Long QT Syndrome. This has led to their widespread adoption in clinical practice and inclusion in treatment guidelines. Moreover, beta blockers are generally well-tolerated by patients, with a favorable side effect profile, which further supports their use.

Despite their benefits, there are some limitations associated with beta blockers. They may not be suitable for all patients, particularly those with contraindications such as asthma or certain types of heart block. Additionally, while beta blockers can reduce the risk of cardiac events, they do not address the underlying genetic mutations resp

Global Long QT Syndrome Treatment market size is expected to reach $3.43 billion by 2029 at 11.5%, impact of rising arrhythmia incidence on long qt syndrome treatment market growth

BackgroundElectrocardiographic QT interval prolongation is the most widely used risk marker for ventricular arrhythmia potential and thus an important component of drug cardiotoxicity assessments. Several antimalarial medicines are associated with QT interval prolongation. However, interpretation of electrocardiographic changes is confounded by the coincidence of peak antimalarial drug concentrations with recovery from malaria. We therefore reviewed all available data to characterise the effects of malaria disease and demographic factors on the QT interval in order to improve assessment of electrocardiographic changes in the treatment and prevention of malaria.Methods and findingsWe conducted a systematic review and meta-analysis of individual patient data. We searched clinical bibliographic databases (last on August 21, 2017) for studies of the quinoline and structurally related antimalarials for malaria-related indications in human participants in which electrocardiograms were systematically recorded. Unpublished studies were identified by the World Health Organization (WHO) Evidence Review Group (ERG) on the Cardiotoxicity of Antimalarials. Risk of bias was assessed using the Pharmacoepidemiological Research on Outcomes of Therapeutics by a European Consortium (PROTECT) checklist for adverse drug events. Bayesian hierarchical multivariable regression with generalised additive models was used to investigate the effects of malaria and demographic factors on the pretreatment QT interval. The meta-analysis included 10,452 individuals (9,778 malaria patients, including 343 with severe disease, and 674 healthy participants) from 43 studies. 7,170 (68.6%) had fever (body temperature ≥ 37.5°C), and none developed ventricular arrhythmia after antimalarial treatment. Compared to healthy participants, patients with uncomplicated falciparum malaria had shorter QT intervals (−61.77 milliseconds; 95% credible interval [CI]: −80.71 to −42.83) and increased sensitivity of the QT interval to heart rate changes. These effects were greater in severe malaria (−110.89 milliseconds; 95% CI: −140.38 to −81.25). Body temperature was associated independently with clinically significant QT shortening of 2.80 milliseconds (95% CI: −3.17 to −2.42) per 1°C increase. Study limitations include that it was not possible to assess the effect of other factors that may affect the QT interval but are not consistently collected in malaria clinical trials.ConclusionsAdjustment for malaria and fever-recovery–related QT lengthening is necessary to avoid misattributing malaria-disease–related QT changes to antimalarial drug effects. This would improve risk assessments of antimalarial-related cardiotoxicity in clinical research and practice. Similar adjustments may be indicated for other febrile illnesses for which QT-interval–prolonging medications are important therapeutic options.

Meta-analysis results from the QT-IGC meta-analysis of QT interval duration. The manuscript detailing the generation and analysis of these results can be found here (https://www.nature.com/articles/ng.3014, Nature Genetics) and here (https://paperpile.com/shared/JEVaXW).

Column names:

1. SNP - SNP identifier (note that these will be on a much older dbSNP build!)
2. CHR - Chromosome
3. POS - Position, hg18
4. A1 - minor allele in HapMap 2
5. A2 - other allele in HapMap 2
6. HAPMAP_A1_FREQ - frequency of A1 in HapMap
7. CODED_ALLELE - the coded allele in the meta. All stats refer to this allele.
8. NONCODED_ALLELE - other allele
9. CODED_ALLELE_FREQ - frequency of the coded allele
10. N_EFF - effective sample size
11. Z_SQRTN - Z-score of the SNP in sample size meta-analysis
12. P_SQRTN - P-value of the SNP in sample size meta-analysis
13. BETA_FIXED - Beta of coded allele in fixed effects meta-analysis
14. SE_FIXED - standard error of coded allele in fixed effects meta-analysis
15. Z_FIXED - z-score of coded allele in fixed effects meta-analysis
16. P_FIXED - p-value in fixed effects meta-analysis
17. BETA_LOWER_FIXED - lower estimate of the beta, fixed effects
18. BETA_UPPER_FIXED - upper estimate of the beta, fixed effects
19. BETA_RANDOM - beta of coded allele in random effects meta-analysis
20. SE_RANDOM - standard error of the coded allele in random effects meta-analysis
21. Z_RANDOM - z-score from random effects meta-analysis
22. P_RANDOM - p-value from random effects meta-analysis
23. BETA_LOWER_RANDOM - lower estimate of the beta, random effects meta
24. BETA_UPPER_RANDOM - upper estimate of the beta, random effects meta
25. COCHRANS_Q - Cochran's test of heterogeneity, Q statistic
26. DF - degrees of freedom for Cochran's Q test
27. P_COCHRANS_Q - p-value of Cochran's Q test
28. I_SQUARED - I-squared stat, test of heterogeneity
29. TAU_SQUARED - Tau-squared, test of heterogeneity
30. DIRECTIONS - directions of the beta in each of the cohorts used in meta-analysis. Cohorts are in the same order as in the params file provided in the related GitHub repo (https://github.com/saralpulit/QTIGCmeta)
31. GENES_1000KB - Genes within 1000kb of the SNP, according to RefSeq
32. NEAREST_GENE - Gene closest to the SNP, according to RefSeq
33. FUNCTION - function of the SNP, if relevant
34. CAVEAT - any relevant caveats, e.g., A/T or C/G SNPs with >40% minor allele frequency

This dataset includes QTc and RR values related to the electrocardiogram of rats exposed to either air or diesel exhaust. This dataset is associated with the following publication: Hazari , M., J. Lancaster, J. Starobin, A. Farraj , and W. Cascio. Diesel exhaust worsens cardiac conduction instability in dobutamine-challenged Wistar-Kyoto and spontaneously hypertensive rats. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 120-129, (2017).

IntroductionThe prognostic impact of QT interval prolongation has not been well studied in healthy Asians. We investigated the association between the QT interval with mortality and cardiovascular events in a healthy Southeast Asian population.MethodsThe QT interval corrected for heart rate using the Bazett’s formula (QTc) was measured in 2536 (825 men, mean age 65.7±7.5 years) Singaporean adults free of cardiovascular disease in the population-based Singapore Longitudinal Ageing Study. Outcomes were all-cause mortality and incident cardiovascular events (cardiovascular mortality, myocardial infarction (MI) and/or stroke).ResultsOver a mean 7.78 years (19695 person-years) of follow-up, there were 202 deaths (45 from cardiovascular causes), 62 cases of myocardial infarction and 64 cases of stroke. Adjusting for age, sex, and cardiovascular risk factors, QTcB prolongation remained independently associated with increased all-cause mortality (HR(per standard deviation) 1.27 (1.10–1.48), p = 0.0015), as well as increased risk of cardiovascular events (HR 1.20 (1.01–1.43), p = 0.0415) and MI/stroke (HR 1.22 (1.01–1.47), p = 0.0455), but not cardiovascular mortality alone (HR 1.05 (0.77–1.44), p = 0.7562).ConclusionsWe provide the first community-based estimates of the independent association of QT prolongation with all-cause mortality and cardiovascular events in Southeast Asians.

Protein-Protein, Genetic, and Chemical Interactions for Wolpert C (2005):Further insights into the effect of quinidine in short QT syndrome caused by a mutation in HERG. curated by BioGRID (https://thebiogrid.org); ABSTRACT: The principal aim of this study was to assess the efficacy of quinidine in suppressing IKr in vitro and in modulating the rate dependence of the QT interval in the "SQT1" form of the short QT syndrome.Graded-intensity bicycle exercise testing was performed off drug in three patients and during oral quinidine in two patients with short QT syndrome and compared to a control group of healthy normal subjects. The in vitro effects of quinidine on currents in patch clamp technique were investigated. Off drugs QTpV3/heart rate correlation is much weaker in patients with short QT syndrome, and QTpV3 shortens less with heart rate increase compared to normal subjects. In addition to prolonging the QT interval into the normal range, quinidine restored the heart rate dependence of the QT interval toward a range of adaptation reported for normal subjects. Data from heterologous expression of wild-type and mutant HERG genes indicate the mutation causes a 20-fold increase in IC50 of d-sotalol but only a 5.8-fold increase in IC50 of quinidine.Oral quinidine is effective in suppressing the gain of function in IKr responsible for some cases of short QT syndrome with a mutation in HERG and thus restoring normal rate dependence of the QT interval and rendering ventricular tachycardia/ventricular fibrillation noninducible.

The purpose of this phase 2, open-label, single-arm, multidose, multicenter study is to investigate the effects of Orteronel plus Prednisone on the QT/QTc interval in patients with Metastatic Castration-Resistant Prostrate Cancer

Protein-Protein, Genetic, and Chemical Interactions for Shimizu W (2000):Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome. curated by BioGRID (https://thebiogrid.org); ABSTRACT: Brugada syndrome is characterized by an ST segment elevation in leads V1-V3 and a high incidence of ventricular fibrillation (VF). A mutation in a cardiac Na+ channel gene, SCN5A, has been linked to Brugada syndrome, and sodium channel blockers have been shown to be effective in unmasking the syndrome when concealed. The aim of this study was to examine the effects of Na+ channel blockers on ST segment elevation, QRS, corrected QT (QTc) interval, and ventricular arrhythmias in patients with Brugada syndrome.We examined the effects of three different Na+ channel blockers (flecainide, disopyramide, and mexiletine) on the amplitude of the ST segment 20 msec after the end of QRS (ST20), QRS duration, QTc interval measured from 12-lead ECG, and ventricular arrhythmias in 12 Brugada and 10 control patients. Maximum ST20 observed in the V2 or V3 leads under baseline conditions was greater in the Brugada patients than in control patients, whereas QRS duration and maximum QTc interval were no different between the two groups. Flecainide and disopyramide, but not mexiletine, significantly increased maximum ST20 and QRS duration in both groups, although these effects were much more pronounced in the Brugada patients. The increases in ST20 and QRS duration with flecainide were significantly larger than those with disopyramide. An increase of 0.15 mV in ST20 with flecainide separated the two groups without overlap. Ventricular premature complexes developed only with flecainide in Brugada patients (3/12) displaying a marked ST elevation but not widening of QRS.Our findings suggest that Na+ channel blockers amplify existing I(Na) and possibly other ion channel defects, with a potency inversely proportional to the rate of dissociation of the drug from the Na+ channel, thus causing a prominent elevation of the ST segment and, in some cases, prolongation of QRS duration in patients with Brugada syndrome.

Four QT prolongation inducers (Terfenadine, Cisapride, Astemizole and Haloperidiol) and 2 non-QT prolongation inducers (Digitoxin and Nitrendipine) were tested on 48 hpf zebrafish embryos. Predominant observed effects are indicated: normal heart rate (N), bradycardia (B), 2∶1 arrhythmia (A), ventricle failure (VF), heart failure (HF).

Beta is in ms. SE = standard error;P* is the P value for the interaction term. Bold indicates significant association for QT interval.

Abstract Ranolazine (RANO) prevents cardiac arrhythmia by blocking the late sodium current (INaL). A transmural gradient of Nav1.5 is found in the left ventricular wall of the heart. Thus, we investigated the effects of RANO in healthy cardiomyocytes and in a cellular model of type 3 long QT syndrome (LQT3). We used isolated endocardium (ENDO) and epicardium (EPI) cells and a video edge detection system and fluorescence microscopy to monitor calcium transients. RANO (0.1, 1, 10 and 30 uM, at 25oC) at a range of pacing frequencies showed a minor impact on both cell types, but RANO at 30uM and 35oC for ENDO cells attenuated sarcomere shortening by~21%. Next, to mimic LQT3, we exposed ENDO and EPI cells to anemone toxin II (ATX-II), which augments INaL. Cellular arrhythmias induced by ATX-II were abrogated by RANO (30 µM) at 35oC. Based on our results we can conclude that RANO has a minor impact on sarcomere shortening of healthy ENDO and EPI cells and it abrogates arrhythmias induced by INaLto a similar level in ENDO and EPI cells.

IntroductionCongenital Long QT Syndrome (LQTS) is common in a First Nations community in Northern British Columbia due to the founder variant KCNQ1 p.V205M. Although well characterized molecularly and clinically in adults, no data have been previously reported on the pediatric population. The phenotype in adults has been shown to be modified by a splice site variant in KCNQ1 (p.L353L). The CPT1A p.P479L metabolic variant, also common in Northern Indigenous populations, is associated with hypoglycemia and infant death. Since hypoglycemia can affect the corrected QT interval (QTc) and may confer risk for seizures (also associated with LQTS), we sought to determine the effect of all three variants on the LQTS phenotype in children within our First Nations cohort.MethodsAs part of a larger study assessing those with LQTS and their relatives in a Northern BC First Nation, we assessed those entering the study from birth to age 18 years. We compared the corrected peak QTc and potential cardiac events (syncope/seizures) of 186 children from birth to 18 years, with and without the KCNQ1 (p.V205M and p.L353L) and CPT1A variants, alone and in combination. Linear and logistic regression and student t-tests were applied as appropriate.ResultsOnly the KCNQ1 p.V205M variant conferred a significant increase in peak QTc 23.8 ms (p 

IntroductionCongenital Long QT Syndrome (LQTS) is common in a First Nations community in Northern British Columbia due to the founder variant KCNQ1 p.V205M. Although well characterized molecularly and clinically in adults, no data have been previously reported on the pediatric population. The phenotype in adults has been shown to be modified by a splice site variant in KCNQ1 (p.L353L). The CPT1A p.P479L metabolic variant, also common in Northern Indigenous populations, is associated with hypoglycemia and infant death. Since hypoglycemia can affect the corrected QT interval (QTc) and may confer risk for seizures (also associated with LQTS), we sought to determine the effect of all three variants on the LQTS phenotype in children within our First Nations cohort.MethodsAs part of a larger study assessing those with LQTS and their relatives in a Northern BC First Nation, we assessed those entering the study from birth to age 18 years. We compared the corrected peak QTc and potential cardiac events (syncope/seizures) of 186 children from birth to 18 years, with and without the KCNQ1 (p.V205M and p.L353L) and CPT1A variants, alone and in combination. Linear and logistic regression and student t-tests were applied as appropriate.ResultsOnly the KCNQ1 p.V205M variant conferred a significant increase in peak QTc 23.8 ms (p 

Effective chemical compound toxicity screening is of paramount importance for safe cardiac drug development. Using mammals in preliminary screening for detection of cardiac dysfunction by electrocardiography (ECG) is costly and requires a large number of animals. Alternatively, zebrafish embryos can be used as the ECG waveform is similar to mammals, a minimal amount of chemical is necessary for drug testing, while embryos are abundant, inexpensive and represent replacement in animal research with reduced bioethical concerns. We demonstrate here the utility of pre-feeding stage zebrafish larvae in detection of cardiac dysfunction by electrocardiography. We have optimised an ECG recording system by addressing key parameters such as the form of immobilization, recording temperature, electrode positioning and developmental age. Furthermore, analysis of 3 days post fertilization (dpf) zebrafish embryos treated with known QT prolonging drugs such as terfenadine, verapamil and haloperidol led to reproducible detection of QT prolongation as previously shown for adult zebrafish. In addition, calculation of Z-factor scores revealed that the assay was sensitive and specific enough to detect large drug-induced changes in QTc intervals. Thus, the ECG recording system is a useful drug-screening tool to detect alteration to cardiac cycle components and secondary effects such as heart block and arrhythmias in zebrafish larvae before free feeding stage, and thus provides a suitable replacement for mammalian experimentation.

AimsShort QT syndrome (SQTS) is an inherited disorder associated with abnormally abbreviated QT intervals and an increased incidence of atrial and ventricular arrhythmias. SQT1 variant (linked to the rapid delayed rectifier potassium channel current, IKr) of SQTS, results from an inactivation-attenuated, gain-of-function mutation (N588K) in the KCNH2-encoded potassium channels. Pro-arrhythmogenic effects of SQT1 have been well characterized, but less is known about the possible pharmacological antiarrhythmic treatment of SQT1. Therefore, this study aimed to assess the potential effects of E-4031, disopyramide and quinidine on SQT1 using a mathematical model of human ventricular electrophysiology.MethodsThe ten Tusscher et al. biophysically detailed model of the human ventricular action potential (AP) was modified to incorporate IKr Markov chain (MC) formulations based on experimental data of the kinetics of the N588K mutation of the KCNH2-encoded subunit of the IKr channels. The modified ventricular cell model was then integrated into one-dimensional (1D) strand, 2D regular and realistic tissues with transmural heterogeneities. The channel-blocking effect of the drugs on ion currents in healthy and SQT1 cells was modeled using half-maximal inhibitory concentration (IC50) and Hill coefficient (nH) values from literatures. Effects of drugs on cell AP duration (APD), effective refractory period (ERP) and pseudo-ECG traces were calculated. Effects of drugs on the ventricular temporal and spatial vulnerability to re-entrant excitation waves were measured. Re-entry was simulated in both 2D regular and realistic ventricular tissue.ResultsAt the single cell level, the drugs E-4031 and disopyramide had hardly noticeable effects on the ventricular cell APD at 90% repolarization (APD90), whereas quinidine caused a significant prolongation of APD90. Quinidine prolonged and decreased the maximal transmural AP heterogeneity (δV); this led to the decreased transmural heterogeneity of APD across the 1D strand. Quinidine caused QT prolongation and a decrease in the T-wave amplitude, and increased ERP and decreased temporal susceptibility of the tissue to the initiation of re-entry and increased the minimum substrate size necessary to prevent re-entry in the 2D regular model, and further terminated re-entrant waves in the 2D realistic model. Quinidine exhibited significantly better therapeutic effects on SQT1 than E-4031 and disopyramide.ConclusionsThe simulated pharmacological actions of quinidine exhibited antiarrhythmic effects on SQT1. This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.

Abstract Background: Trimetazidine (TMZ) is an anti-ischemic drug. In spite of its protective effects on cardiovascular system, there is no scientific study on the usefulness of TMZ treatment for prolonged QT interval and cardiac hypertrophy induced by diabetes. Objectives: To evaluate the effects of TMZ on QT interval prolongation and cardiac hypertrophy in the diabetic rats. Methods: Twenty-four male Sprague-Dawley rats (200-250 g) were randomly assigned into three groups (n = 8) by simple random sampling method. Control (C), diabetic (D), and diabetic administrated with TMZ at 10 mg/kg (T10). TMZ was administrated for 8 weeks. The echocardiogram was recorded before isolating the hearts and transfer to a Langendorff apparatus. Hemodynamic parameters, QT and corrected QT interval (QTc) intervals, heart rate and antioxidant enzymes were measured. The hypertrophy index was calculated. The results were evaluated by one-way ANOVA and paired t-test using SPSS (version 16) and p < 0.05 was regarded as significant. Results: The diabetic rats significantly indicated increased hypertrophy, QT and QTc intervals and decreased Left ventricular systolic pressure (LVSP), Left ventricular developed pressure (LVDP), rate pressure product (RPP), Max dp/dt, and min dp/dt (±dp/dt max), heart rate, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in the heart. Treatment with TMZ in the diabetic animals was significantly improved these parameters in comparison to the untreated diabetic group. Conclusions: TMZ improves QTc interval prolongation and cardiac hypertrophy in diabetes.

Predicted QT intervals at baseline and in recovery from malaria and fever.