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Dive into the research topics where Janos Molnar is active.

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Featured researches published by Janos Molnar.


American Journal of Cardiology | 1997

Relation of left ventricular mass and QT dispersion in patients with systematic hypertension

Khachig Ichkhan; Janos Molnar; John C. Somberg

This study evaluated the correlation of left ventricular hypertrophy and QT dispersion in patients with systemic hypertension. QT dispersion, determined using the standard electrocardiogram, showed an increase as left ventricular mass determined by echocardiography increased in hypertensive patients.


Catheterization and Cardiovascular Interventions | 2004

Validation of a new formula for mean arterial pressure calculation: The new formula is superior to the standard formula

Mansour Razminia; Atul Trivedi; Janos Molnar; Monther Elbzour; Mayra Guerrero; Yasser Salem; Aziz Ahmed; Sandeep Khosla; David L. Lubell

Mean arterial pressure (MAP) has traditionally been derived from systolic and diastolic pressures, weighted 1/3 systolic and 2/3 diastolic. No correction is made for the increasing time dominance of systole with increasing heart rates. In a previous study, we developed a new and more accurate heart rate‐corrected MAP formula from central aorta pressure determinations in a large number of patients: MAP = DP + [0.33 + (HR × 0.0012)] × [PP] where SP and DP are systolic and diastolic pressure and HR is heart rate. The current study validates the new MAP formula in the same patient at increasing paced heart rates. A central aorta catheter was used to obtain computer‐determined systolic, diastolic, and MAP in 12 patients. Values were obtained at baseline and then at increasing right atrial paced heart rates. The new and standard MAP formula‐derived values were compared with computer‐determined values. The new formula showed a much closer correlation with the computer‐derived values for MAP. Standard MAP calculations for MAP can easily be improved by inclusion of a heart rate factor. Catheter Cardiovasc Interv 2004;63:419–425.


Journal of Cardiovascular Pharmacology and Therapeutics | 2010

Effect of Niacin Therapy on Cardiovascular Outcomes in Patients With Coronary Artery Disease

Jasleen Duggal; Mukesh Singh; Navneet Attri; Param Singh; Neyaz Ahmed; Suneet Pahwa; Janos Molnar; Sarabjeet Singh; Sandeep Khosla; Rohit Arora

Background: Niacin or nicotinic acid (vitamin B3) raises the levels of high-density lipoprotein cholesterol (HDL) by about 30% to 35%. In patients with prior coronary disease, 7 trials have been published on clinical cardiovascular disease outcomes and the results, not surprisingly, are inconsistent. Hence, we performed this meta-analysis of randomized placebo-controlled trials (RCTs) to evaluate the effect of niacin on cardiovascular outcomes in patients with coronary artery disease. Methods: A systematic search using PubMed, EMBASE, and Cochrane library databases was performed. Seven studies with a total of 5137 patients met our inclusion criteria. Heterogeneity of the studies was analyzed by the Cochran Q statistics. The significance of common treatment effect was assessed by computing the combined relative risks using the Mantel-Haenszel fixed-effect model. A 2-sided alpha error of less than .05 was considered statistically significant (P < .05). Results: Compared to placebo group, niacin therapy significantly reduced coronary artery revascularization (RR [relative risk]: 0.307 with 95% CI: 0.150-0.628; P = .001), nonfatal myocardial infarction ([MI]; RR: 0.719; 95% CI: 0.603-0.856; P = .000), stroke, and TIA ([transient ischemic attack] RR: 0.759; 95%CI: 0.613-0.940; P = .012), as well as a possible but nonsignificant decrease in cardiac mortality (RR: 0.883: 95% CI: 0.773-1.008; p= 0.066). Conclusions: In a meta-analysis of seven trials of secondary prevention, niacin was associated with a significant reduction in cardiovascular events and possible small but non-significant decreases in coronary and cardiovascular mortality.


International Journal of Cardiology | 2010

Bisphosphonate use in women and the risk of atrial fibrillation: a systematic review and meta-analysis.

Rohit Bhuriya; Mukesh Singh; Janos Molnar; Rohit Arora; Sandeep Khosla

BACKGROUND Bisphosphonates are used for the prevention and treatment of osteoporosis, but there have been concerns about a potential link between bisphosphonate therapy and atrial fibrillation. Data on the effects of bisphosphonate on the risk of atrial fibrillation are conflicting and the association of serious atrial fibrillation (defined as events resulting in hospitalization or disability or judged to be life-threatening) with the use of bisphosphonates is uncertain. HYPOTHESIS We aimed to systematically evaluate the association of bisphosphonate use with the risk of atrial fibrillation. METHODS We performed a systematic literature search for clinical trials using bisphosphonates and providing data on the outcome of atrial fibrillation. Four randomized controlled trials and 3 population based case-control studies were included in the final analysis. A meta-analysis was performed with the 4 randomized controlled trials to determine the risk of serious atrial fibrillation. RESULTS For the purpose of meta-analysis, the studies were homogenous; therefore the Mantel-Haenszel fixed-effect model was used to calculate combined relative risk (RR). A two-sided alpha error of less than 0.05 was considered to be statistically significant (p<0.05). Four studies with 26126 postmenopausal women were included in the meta-analysis. Meta-analysis revealed that serious atrial fibrillation occurred more frequently in the bisphosphonate group compared to the placebo group (RR 1.525; 95% CI, 1.166 to 1.997; p=0.002). Two out of 3 observational studies indicated a statistically significant increase in the risk of atrial fibrillation with bisphosphonate therapy. CONCLUSIONS Bisphosphonate use is associated with a significant increase in the risk of serious atrial fibrillation in postmenopausal women.


Clinical Cardiology | 2009

Stem cells improve left ventricular function in acute myocardial infarction.

Sarabjeet Singh; Rohit Arora; Kamna Handa; Ahmad Khraisat; Nagapradeep Nagajothi; Janos Molnar; Sandeep Khosla

Animal studies have suggested dramatic improvement in cardiac function after acute myocardial infarction (AMI) through regeneration of the myocardium or neovascularization by transfer of cells derived from bone marrow (BMC) generated clinical studies. Recently published small sized studies have yielded mixed results, leaving the question unanswered.


Canadian Journal of Cardiology | 2007

Cocaine-related acute aortic dissection: patient demographics and clinical outcomes.

Sarabjeet Singh; Atul Trivedi; Tara Adhikari; Janos Molnar; Rohit Arora; Sandeep Khosla

BACKGROUND To compare the demographics, inpatient mortality and short-term survival following hospital discharge between cocaine-using and non-cocaine-using patients presenting with acute aortic dissection. METHODS Retrospective analysis of 46 consecutive patients admitted with the diagnosis of acute aortic dissection at the Mount Sinai Hospital (Chicago, USA) between 1996 and 2005. Among these 46 patients, cocaine use was temporally related to the presenting symptom in 13 patients (28%, group 1). Patients who were not cocaine users were grouped into group 2 (33 patients [72%]). RESULTS Patients in group 1 were younger than those in group 2 (mean age 38+/-9 years versus 63+/-17 years, P=0.001), more likely to be smokers (13 of 13 patients [100%] versus 15 of 33 patients [45%], P=0.001) and had a higher prevalence of accelerated hypertension (mean blood pressure 210/130 mmHg) compared with group 2 (10 of 13 patients [77%] versus 11 of 33 patients [33%]) (P=0.01). Group 1 patients had a higher prevalence of type B dissection than group 2 (nine of 13 patients [69%] versus one of 33 patients [3%]). After hospital discharge, eight of 13 patients (62%) in the cocaine group continued to use cocaine. Mortality following hospital discharge was significantly higher in cocaine users (nine of 13 patients [69%]) compared with the non-cocaine users (four of 33 patients [12%], P=0.01). Recurrent dissection was the cause of death in five of the 13 deaths (42%) in the cocaine group. CONCLUSIONS Patients presenting with acute aortic dissection temporally related to cocaine use are more likely to be younger, smokers, have higher prevalence of hypertensive crises, more likely to have type B aortic dissection and may have a higher mortality following hospital discharge, possibly due to continued cocaine use and recurrent aortic dissection.


American Journal of Therapeutics | 2001

Influence of electrolyte abnormalities on interlead variability of ventricular repolarization times in 12-lead electrocardiography.

Yelamanchi Vp; Janos Molnar; Ranade; John C. Somberg

Increased QT dispersion (QTd) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QTd. Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JTd), and QTc (QTcd) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QTd (115 ± 31 vs. 49 ± 15 ms), JTd (116 ± 34 vs. 52 ± 12 ms), and QTcd (141 ± 40 vs. 58 ± 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K+ and seven on Mg2+-free diet followed by normal diet. Experimental hypokalemia significantly increased QTd (10 ± 4 to 37 ± 7 ms), and QTcd (32 ± 6 to 79 ± 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QTd, 14 ± 2; QTcd, 34 ± 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.


American Journal of Cardiology | 2002

Differential effect of glyburide (Glibenclamide) and metformin on QT dispersion : A potential adenosine triphosphate sensitive K+ channel effect

Syed A. Najeed; Ijaz A. Khan; Janos Molnar; John C. Somberg

Glyburide (glibenclamide) is a specific blocker of the adenosine triphosphate (ATP) sensitive potassium (K+) channel. It has been reported to result in prolongation of the QT interval. QT interval dispersion (QTd) is a potentially sensitive marker for increased risk of arrhythmia and sudden cardiac death. The aim of the present study was to evaluate the effect of glyburide on QTd and compare it with that of metformin, a hypoglycemic agent that does not block the adenosine triphosphate sensitive K+ channel. Thirty patients with type 2 diabetes were randomized to glyburide and metformin groups. A 12-lead electrocardiogram was obtained before and at 2 months after being on glyburide or metformin. Therapy with QT and QTd were measured and QT corrected for rate (QTc). There was no significant difference between the glyburide and metformin groups in age (62 +/- 9 vs 59 +/- 10 years), baseline RR interval (819 +/- 86 vs 753 +/- 100 ms), QT (387 +/- 28 vs 383 +/- 27 ms), and QTc (433 +/- 25 vs 444 +/- 15 ms). Glyburide was associated with a significant increase in QTc (433 +/- 24 to 467 +/- 24 ms, p <0.001), QTd (24 +/- 16 to 60 +/- 22 ms, p <0.001), and QTc dispersion (QTcd) (35 +/- 18 to 68 +/- 21 ms, p <0.001). In contrast, metformin was associated with a decrease in QTc (444 +/- 15 to 432 +/- 15 ms, p <0.01) and did not affect QTd (14 +/- 5 to 12 +/- 6 ms, p = NS) and QTcd (23 +/- 9 to 22 +/- 10 ms, p = NS). Glyburide, unlike metformin, causes an increase in QT dispersion. Increased dispersion may be a factor underlying an increased risk of arrhythmias and sudden cardiac death.


Clinical Cardiology | 2013

Associations between sleep duration and prevalence of cardiovascular events.

Saurabh Aggarwal; Rohit S. Loomba; Rohit Arora; Janos Molnar

Data regarding the associations between sleep duration and clinical cardiovascular (CV) events are limited. We aimed to analyze any associations between self‐reported sleep duration and CV events.


Journal of Clinical Hypertension | 2011

Effects of Statins on Progression of Coronary Artery Disease as Measured by Intravascular Ultrasound

Updesh Singh Bedi; Mukesh Singh; Param Singh; Janos Molnar; Sandeep Khosla; Rohit Arora

J Clin Hypertens (Greenwich). 2011;13:492–496.©2011 Wiley Periodicals, Inc.

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Rohit Arora

Rosalind Franklin University of Medicine and Science

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John C. Somberg

Rush University Medical Center

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Sandeep Khosla

Rosalind Franklin University of Medicine and Science

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Sarabjeet Singh

Rosalind Franklin University of Medicine and Science

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Mukesh Singh

Rosalind Franklin University of Medicine and Science

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V. Ranade

Rush University Medical Center

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Rohit Bhuriya

Rosalind Franklin University of Medicine and Science

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Rohit Arora

Rosalind Franklin University of Medicine and Science

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Aarthi Ganesh

Rosalind Franklin University of Medicine and Science

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