Jan Klimas

Publications (13)26.22 Total impact

• Article: Glucose and blood pressure lowering effects of Pycnogenol® are inefficient to prevent prolongation of QT interval in experimental diabetic cardiomyopathy.

  Stanislava Jankyova, Jana Kmecova, Hana Cernecka, Lucia Mesarosova, Peter Musil, Zuzana Brnoliakova, Jan Kyselovic, Pavel Babal, Jan Klimas
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  ABSTRACT: Diabetic cardiomyopathy shows ECG alterations related to cardiac repolarization and manifested by increased duration of QT interval. Although the mechanism is unknown, it is widely believed that the reduction of hyperglycaemia might prevent such alterations. To test this hypothesis, we used the standardized extract of French pine bark - Pycnogenol(®) (PYC) with hypoglycaemic and antioxidant properties in 8-9 week old rats with experimentally (streptozotocin) induced diabetes mellitus (DM). PYC was administered orally for 6 weeks in three different doses (10, 20, and 50 mg/kg b.w., resp.). Experimental DM was manifested by hyperglycaemia (four to six-fold increase in plasma glucose concentration; p<0.05) and significantly increased mean arterial blood pressure (by 19%; p<0.05) measured using catheterization of carotid artery in vivo. Both abnormalities were dose-dependently reduced by PYC. In addition, diabetic cardiomyopathy was associated with a significant increase in left ventricular weight to body weight ratio (by 21%; p<0.05) and a significant decrease of the width of cardiomyocytes (by 23%; p<0.05) indicating cardiac edema on the one side, and hypotrophy of cardiomyocytes on the other. Both of these changes were not affected by PYC. Consequently to metabolic and hemodynamic alterations, significant prolongation of QT interval (by 20%; p<0.05) was present in diabetic rats, however, PYC failed to correct it. Conclusively, PYC fails to correct QT prolongation in spite of dose-dependent reduction of glycaemia and high blood pressure in streptozotocin-induced diabetic cardiomyopathy.
  Pathology - Research and Practice 06/2012; 208(8):452-7. · 1.21 Impact Factor
• Article: Discrepant Regulation of QT (QTc) Interval Duration by Calcium Channel Blockade and Angiotensin Converting Enzyme Inhibition in Experimental Hypertension.

  Jan Klimas, Vaclav Vaja, Miriam Vercinska, Jan Kyselovic, Peter Krenek
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  ABSTRACT: Antihypertensive treatment may reduce prolonged QT duration in hypertension. Generally, the reductions of blood pressure and/or of cardiac mass are believed to be the responsible factors. However, drugs are not equivalent in QT modulation despite similar antihypertensive and antihypertrophic action. We investigated the effect of a calcium channel blocker, lacidipine and an angiotensin-converting enzyme inhibitor, enalapril on QT duration in rats. Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were treated with lacidipine (at the dose of 1.5 mg/kg per day for WKY and 3 mg/kg per day for SHR) or enalapril (5 mg/kg per day for WKY and 10 mg/kg per day for SHR) during 8 weeks. Tail-cuff systolic blood pressure (sBP), left ventricular weight (LVW), vascular function of isolated aorta and mesenteric artery and duration of QT (and QTc) interval on Frank electrocardiograms were evaluated. As expected, untreated SHR showed elevated sBP, impaired vascular reactivity, increased LVW and prolonged QT when compared with WKY (p < 0.05). After treatment, both agents markedly improved vascular reactivity and reduced sBP in SHR (p < 0.05). Additionally, enalapril reduced LVW in both hypertensive (by 17%; p < 0.05) and normotensive rats (by 13%; p < 0.05) and, consequently, corrected QT duration in SHR. Interestingly, lacidipine also reduced LVW in SHR (by 9%; p < 0.05), but without influence on prolonged QT. Moreover, lacidipine had no effect on LVW in WKYs but prolonged their QT interval (by 10%; p < 0.05). In conclusion, lacidipine did not reverse a progressive prolongation of QT in SHR, despite sBP lowering and LVW reduction. Thus, the lowering of blood pressure and/or reduction of LVW are not sufficient per se to normalize ventricular repolarization in hypertensive cardiac disease. More likely, modulation of QT prolongation by antihypertensive drugs is a function of their complex action on blood pressure, vascular function, cardiac mass and on reflex neurohumoral activation.
  Basic & Clinical Pharmacology & Toxicology 05/2012; 111(4):279-88. · 2.18 Impact Factor
• Article: Enalapril decreases cardiac mass and fetal gene expression without affecting the expression of endothelin-1, transforming growth factor β-1, or cardiotrophin-1 in the healthy normotensive rat.

  Katarina Mackovicova, Andrea Gazova, Dana Kucerova, Beata Gajdacova, Jan Klimas, Peter Ochodnicky, Eva Goncalvesova, Jan Kyselovic, Peter Krenek
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  ABSTRACT: Angiotensin II can induce cardiac hypertrophy by stimulating the release of growth factors. ACE inhibitors reduce angiotensin II levels and cardiac hypertrophy, but their effects on the healthy heart are largely unexplored. We hypothesized that ACE inhibition decreases left ventricular mass in normotensive animals and that this is associated with altered expression of cardiac fetal genes, growth factors, and endothelial nitric oxide synthase (eNOS). Wistar rats (n = 7 per group) were orally administered with enalapril twice daily for a total daily dose of 5 mg·kg(-1)·d(-1) (ENAP5) or 15 mg·kg(-1)·d(-1) (ENAP15) or vehicle. Systolic blood pressure was measured by the tail-cuff method. Left ventricular expression of cardiac myosin heavy chain-α (MYH6) and -β (MYH7), atrial natriuretic peptide (ANP), endothelin-1 (ET-1), transforming growth factor β-1 (TGFβ-1), cardiotrophin-1 (CT-1), and renal renin were examined by real-time PCR, and eNOS using Western blot. Blood pressure was decreased only in ENAP15 animals (p < 0.05 vs. Control), whereas left ventricular mass decreased after both doses of enalapril (p < 0.05 vs. Control). MYH7 and ANP were reduced in ENAP15, while no changes in ET-1, TGFβ-1, CT-1, and MYH6 mRNA or eNOS protein were observed. Renal renin dose-dependently increased after enalapril treatment. Enalapril significantly decreased left ventricular mass even after 1 week treatment in the normotensive rat. This was associated with a decreased expression of the fetal genes MYH7 and ANP, but not expression of ET-1, CT-1, or TGFβ-1.
  Canadian Journal of Physiology and Pharmacology 03/2011; 89(3):197-205. · 1.95 Impact Factor
• Article: Heart rate correction of the QT duration in rats.

  Jana Kmecova, Jan Klimas
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  ABSTRACT: Duration of heart rate corrected QT interval (QTc) is a crucial and critical factor in the assessment of repolarization changes considering safety of drugs and cardiac disorders. In rats, a validated approach to QT correction is lacking. In this study, we tested the normalization of QTc using normalization factor according to rat's cardiac cycle length (RR). Standard 12-lead ECG was measured in anesthetized rats at basal conditions and at various pharmacological conditions such as beta-adrenergic stimulation with isoproterenol or medication with clarithromycin (single- or repeated dosing for seven days), bisoprolol or ivabradine. For QT correction, standard Bazett's formula (QTc-B=QT/(RR)(1/2)) and Bazett's formula normalized to average rat RR (QTc(n)-B=QT/(RR/f)(1/2), f=150ms) were compared. Duration of QT showed a positive correlation with RR duration (Pearson r=0.7645, P<0.001). Calculated QTc-B gave 2-2.5 fold of values of uncorrected QT, whereas values of normalized QTc(n)-B were in the physiological range. QTc(n)-B was unrelated to RR (Pearson r=0.1122, not significant) but the relationship between QTc(n)-B and QT remained preserved (Pearson r=0.7216, P<0.001). Both single and repeated administration of clarithromycin prolonged QT as compared to the controls but a significant dose-dependent difference between clarithromycin applications was revealed only when QTc(n)-B was used. Beta-adrenergic stimulation with isoproterenol prolonged, while beta-blockade with bisoprolol shortened QTc(n)-B. Ivabradine dose-dependently induced bradycardia without altering QT. However, QTc(n)-B showed false positive shortening at sustained bradycardia. Therefore, adjusted formula for QTc(n)-B is suitable for QT correction in rats but its use should be considered carefully in case of very low heart rate.
  European journal of pharmacology 09/2010; 641(2-3):187-92. · 2.59 Impact Factor
• Article: Pycnogenol improves left ventricular function in streptozotocin-induced diabetic cardiomyopathy in rats.

  Jan Klimas, Jana Kmecova, Stanislava Jankyova, Diana Yaghi, Elena Priesolova, Zuzana Kyselova, Peter Musil, Peter Ochodnicky, Peter Krenek, Jan Kyselovic, Stefan Matyas
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  ABSTRACT: We studied whether Pycnogenol (PYC) may attenuate the development of experimental streptozotocin-induced diabetic cardiomyopathy in rat. In addition, we aimed to study whether PYC affects cardiac oxidative stress and the protein expression of reactive oxygen species (ROS)-producing molecules (gp91(phox)-containing NADPH oxidase and NO-signalling proteins). Experimental diabetes mellitus was manifested by hyperglycaemia and impaired cardiac function estimated using left ventricular catheterisation in vivo. PYC lowered fasting plasma glucose and normalized basal cardiac function. Excessive oxidative stress in streptozotocin (STZ) hearts, evidenced by 40% increase (P < 0.05) of thiobarbituric acid reactive substances (TBARS) concentration, was associated with increased expression of gp91(phox) (by 75%, P < 0.05), iNOS (by 40%, P < 0.05) and alpha-tubulin (by 49%, P < 0.05), but unchanged expression of eNOS and its alosteric regulators, as compared to CON. PYC failed to affect these expression abnormalities. Our study shows that PYC corrects diabetic cardiac dysfunction, probably by its metabolic and direct radical scavenging activity without affecting the molecular maladaptations of ROS-producing enzymes and cytoskeletal components.
  Phytotherapy Research 12/2009; 24(7):969-74. · 2.09 Impact Factor
• Article: Rapid large artery remodeling following the administration and withdrawal of calcium channel blockers in spontaneously hypertensive rats.

  Vaclav Vaja, Peter Ochodnicky, Peter Krenek, Jan Klimas, Zuzana Bajuszova, Jan Kyselovic
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  ABSTRACT: Chronic treatment with several antihypertensive agents, including calcium channel blockers, may interfere with remodeling of large arteries and increased arterial stiffness. We hypothesize that even a short, seven-day administration of calcium channel blockers might alter an aortic remodeling in spontaneously hypertensive rat (SHR). Male SHR and normotensive WKY rats (n=14 each) were treated by either vehicle, vasculoselective calcium channel blocker nifedipine (1mg/kg/day) or cardiac/vascular calcium channel blockers diltiazem (5mg/kg/day) or verapamil (4 mg/kg/day, n=6 for each treatment) subcutaneously twice daily for seven days. Additional SHR rats were randomized for termination 24, 72 or 120 h (n=5 each) after the withdrawal of nifedipine. Systolic blood pressure was measured by tail cuff and thoracic aorta was collected for histomorphometric and functional analysis including acetylcholine-induced endothelium-dependent relaxation. Seven-day administration of diltiazem and nifedipine, but not verapamil decreased blood pressure in SHR. All drugs significantly attenuated abnormal aortic wall thickness, cross-sectional area and media-to-lumen ratio, but only nifedipine improved impaired endothelium-dependent relaxation. Following the withdrawal of nifedipine, all measured parameters returned back to control SHR values within 72 h. Seven-day treatment with distinct calcium channel blockers attenuates hypertensive remodeling of aorta, which might be, in case of nifedipine, reactivated even by a very short withdrawal of the drug. Therefore, vasculoprotection by calcium channel blockers is not restricted to a prolonged blood pressure modulation, but occurs rapidly. These findings could be relevant for an intervention in augmented vascular stiffness and related cardiovascular risk.
  European journal of pharmacology 09/2009; 619(1-3):85-91. · 2.59 Impact Factor
• Article: Effect of chronic nNOS inhibition on blood pressure, vasoactivity, and arterial wall structure in Wistar rats.

  Sona Cacanyiova, Frantisek Kristek, Maria Gerova, Peter Krenek, Jan Klimas
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  ABSTRACT: While the unequivocal pattern of endothelial nitric oxide (NO) synthase (eNOS) inhibition in cardiovascular control has been recognised, the role of NO produced by neuronal NOS (nNOS) remains unclear. The purpose of the present study was to describe the cardiovascular effects of NO production interference by inhibition of nNOS with 7-nitroindazole (7-NI). Wistar rats (10 weeks old) were used: control and experimental rats were administered 7-NI 10 mg/kg b.w./day in drinking water for 6 weeks. Systolic blood pressure (BP) was measured by the tail-cuff plethysmographic method. Isolated thoracic aortas (TAs) were used to study vasomotor activity of the conduit artery in vitro. The BP response of anaesthetised animals was used to follow the cardiovascular-integrated response in vivo. Geometry of the TA was measured after perfusion fixation (120 mm Hg) by light microscopy. Expression of eNOS was measured in the TA by immunoblot analysis. Although 6 weeks of nNOS inhibition did not alter systolic BP, the heart/body weight ratio was decreased. Relaxation of the TA in response to acetylcholine (10(-9)-10(-5)mol/L) was moderately inhibited. However, no difference in the BP hypotensive response after acetylcholine (0.1, 1, 10 microg) was observed. The contraction of TA in response to noradrenaline (10(-10)-10(-5)mol/L), and the BP pressor response to noradrenaline (0.1, 1 microg) was attenuated. The inner diameter of the TA was increased, and the wall thickness, wall cross-sectional area, and wall thickness/inner diameter ratio were decreased. The expression of eNOS in the TA was increased. In summary, cardiac and TA wall hypotrophy, underlined by decreased contractile efficiency, were observed. The results suggested that two constitutive forms of NOS (nNOS, eNOS) likely participate in regulation of cardiovascular tone by different mechanisms.
  Nitric Oxide 04/2009; 20(4):304-10. · 3.55 Impact Factor
• Article: Isoproterenol-induced heart failure in the rat is associated with nitric oxide-dependent functional alterations of cardiac function.

  Peter Krenek, Jana Kmecova, Dana Kucerova, Zuzana Bajuszova, Peter Musil, Andrea Gazova, Peter Ochodnicky, Jan Klimas, Jan Kyselovic
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  ABSTRACT: The role of nitric oxide (NO) in heart failure (HF) is complex and remains controversial. We tested the hypothesis that the role of NO in isolated atria and cardiomyocytes is altered in isoproterenol-induced HF. Rats received isoproterenol (ISO, 5 mg/kg/day, intraperitoneally) or vehicle for 1 week. Haemodynamic parameters were obtained by left ventricular catheterization. Effects of NOS inhibition on isolated atria and on electrically paced left ventricular myocytes were determined. Additionally, expressions of nitric oxide synthases and their allosteric modulators hsp90, caveolin-1, and caveolin-3 proteins in the left ventricles were measured. ISO increased left ventricular mass by 33% and decreased indices of left ventricular systolic and diastolic function dp/dtmin and dp/dtmax (both P<0.05). Isolated atria from HF rats had a lower spontaneous beating rate (P<0.05). NOS inhibition by L-NAME increased basal frequency and attenuated the positive chronotropic effect of beta-adrenergic stimulation in the HF group (P<0.05). Ventricular myocytes from failing hearts had impaired cell shortening. L-NAME decreased contractility of control, but not failing myocytes. Left ventricular expressions of eNOS, hsp90, iNOS, but not nNOS or caveolins, were increased. Despite the increased capacity for NO synthesis in isoproterenol-induced HF, NO does not sustain contractility of failing myocytes. NO may contribute to the decreased basal heart rate and it may accelerate beta-adrenergic stimulation of chronotropy.
  European Journal of Heart Failure 02/2009; 11(2):140-6. · 4.90 Impact Factor
• Article: Prolonged QT interval is associated with blood pressure rather than left ventricular mass in spontaneously hypertensive rats.

  Jan Klimas, Tatiana Stankovicova, Jan Kyselovic, Ljuba Bacharova
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  ABSTRACT: QT interval is prolonged in hypertensive individuals, although the factors responsible for this increase are not completely understood. We questioned whether enhanced left ventricular mass (LVM) or increased systemic blood pressure represents the principal factor determining QT prolongation in the period of development of hypertension and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). In 12-and 20-week-old SHR (SHR12 and SHR20) and age-matched normotensive Wistar-Kyoto rats (WKY12 and WKY20), arterial systolic blood pressure (sBP) was measured using tail-cuff technique. Orthogonal Frank ECG was registered in anaesthetized animals in vivo, and bipolar ECG was measured in spontaneously beating isolated hearts in vitro. Progressive increase of sBP and LVM resulted in significant QT prolongation in SHR20 as compared to WKY12, WKY20, and also to SHR12 in vivo (WKY12: 82 +/- 9 ms, WKY20: 81 +/- 9 ms, SHR12: 88 +/- 15 and SHR20: 100 +/- 10, respectively; p < 0.05) but not in isolated hearts (WKY20: 196 +/- 39 ms and SHR20: 220 +/- 55, respectively; NS). In whole animals, QT duration was positively related to sBP (r = 0.6842; p < 0.001) but not to LVM (r = 0.1632, NS) in SHR20. The results suggest that QT prolongation in SHR developing hypertension and LVH depends on blood pressure rather than increase in LVM. In this period, myocardial hypertrophy is probably the predisposition for QT prolongation, but the significant change manifests only in the presence of elevated systemic factors.
  Clinical and Experimental Hypertension 10/2008; 30(7):475-85. · 1.07 Impact Factor
• Article: Discrepancy between increased left ventricular mass and "normal" QRS voltage is associated with decreased connexin 43 expression in early stage of left ventricular hypertrophy in spontaneously hypertensive rats.

  Ljuba Bacharova, Jana Plandorova, Jan Klimas, Peter Krenek, Jan Kyselovic
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  ABSTRACT: On the basis of our previous results of animal and human studies, we assume that the discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) findings not exceeding the upper normal limits in left ventricular hypertrophy (LVH) are conditioned by the electrical remodeling of hypertrophied myocardium. We assumed that these discrepancies observed in the early stage of LVH in spontaneously hypertensive rats (SHR) are associated with a decreased expression of connexin 43. Standard 12-lead ECG was recorded in 20-week-old male SHR and age-matched and sex-matched normotensive Wistar rats (Institute of Experimental Pharmacology SAV, Dobra Voda, Slovakia). The approximated maximum QRS spatial vector magnitude (QRSmax) was calculated from leads V(2), aVF, and V(5). Left ventricular mass was weighed, and the specific potential (SP) of myocardium was calculated as the QRSmax-to-LVM ratio. Left ventricular protein levels of connexin 43 were analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting. The LVM values were significantly higher in SHR than in normotensive controls (0.96 +/- 0.03 g and 0.680 +/- 0.07 g, respectively; P < .001). The QRSmax values in SHR did not follow the increase either in systolic blood pressure or in LVM. The SP values in SHR were significantly lower than those in control rats (0.92 +/- 0.11 mV/g and 1.358 +/- 0.06 mV/g, respectively; P < .01). A 37% decrease in connexin 43 level was observed in SHR. The QRS voltage did not follow the increase in the LVM in 20-week-old SHR, and the values of connexin 43 were lower in SHR than in normotensive controls. We believe that the discrepant findings between ECG voltage and LVM can be caused by the electrical remodeling in the early stages of LVH.
  Journal of electrocardiology 03/2008; 41(6):730-4. · 1.08 Impact Factor
• Article: Relation between QRS amplitude and left ventricular mass in the initial stage of exercise-induced left ventricular hypertrophy in rats.

  Ljuba Bacharova, Karol Michalak, Jan Kyselovic, Jan Klimas
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  ABSTRACT: The aim of the study was to analyze the relationship between QRS amplitude and left ventricular mass (LVM) in early stages of two different experimental models of left ventricular hypertrophy (LVH) in rats: in exercise-induced hypertrophy and pathological hypertrophy due to genetically conditioned pressure overload. Three groups of experimental animals were studied: healthy control Wistar-Kyoto rats (WKYs), spontaneously hypertensive rats (SHRs), and WKY rats exposed to training by intermittent swimming (SWIM). Orthogonal electrocardiograms were recorded in each group at the age of 12 and 20 weeks, and the maximum spatial QRS vector (QRSmax) was calculated. Then the animals were sacrificed and LVM was measured. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The QRSmax values did not follow the changes in LVM. At the end of the follow-up period, the highest values of QRSmax were recorded in the control WKY rats (0.80 +/- 0.05 mV). The QRSmax values in both groups with experimental LVH were significantly lower as compared with control animals (SHR 0.44 +/- 0.02 mV, p < 0.001; SWIM 0.53 +/- 0.04 mV, p < 0.001). Similarly, the SP values were significantly lower in both groups with experimental LVH as compared with control animals (SHR 0.42 +/- 0.02 mV/g, p < 0.001; SWIM 0.55 +/- 0.05 mV/g, p < 0.001). A decrease in QRSmax and SP was observed in both models of experimental LVH. We attributed these findings to the changes in electrogenetic properties of myocardium in the early stage of developing LVH. In other words, it is changes of nonspatial determinants that influence the resultant QRS voltage in terms of the solid angle theory.
  Clinical and Experimental Hypertension 09/2005; 27(6):533-41. · 1.07 Impact Factor
• Article: The initial stage of left ventricular hypertrophy in spontaneously hypertensive rats is manifested by a decrease in the QRS amplitude/left ventricular mass ratio.

  Ljuba Bacharova, Jan Kyselovic, Jan Klimas
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  ABSTRACT: In this study we tested the hypothesis of the relative voltage deficit, i.e. the discrepancy between increased left ventricular mass (LVM) and QRS amplitudes, in an experimental model of spontaneously hypertensive rats (SHR) during the period of a moderate increase in blood pressure. To address this issue we recorded orthogonal electrocardiograms of male SHR at the age of 12 and 20 weeks. During this period the systolic blood pressure (sBP) increased from 165 +/- 3 mmHg to 195 +/- 1 mmHg (p < 0.001). Age and sex matched WKY rats were used as control groups. The sBP values in WKY normotensive control groups were within normal limits (122 +/- 8 mmHg and 130 +/- 4mmHg, respectively). The maximum QRS spatial vector magnitude (QRSmax) was calculated from X, Y, Z amplitudes of the orthogonal electrocardiograms. The animals were sacrificed and the left ventricular mass was weight. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The LVM in SHR (0.86 +/- 0.05 g and 1.05 +/- 0.07 g, respectively) was significantly higher as compared to WKY (0.65 +/- 0.07 g and 0.70 +/- 0.02 g), and the increase of LVM closely correlated with the sBP increase. On the other hand, QRSmax in SHR did not follow either the increase of sBP, or LVM. The QRSmax values in SHR did not differ from those of WKY at the age of 12 weeks (0.59 +/- 0.14 mV compared to 0.46 +/- 0.05 mV), and they were even lower in SHR at the age of 20 weeks (0.74 +/- 0.08 mV compared to 0.44 +/- 0.05 mV, p < 0.001). The values of SP, quantifying the relative voltage deficit, were significantly lower in SHR as compared to the WKY control. The values decreased significantly in SHR with increasing age, sBP and LVM, i.e., with the progression of hypertrophic remodeling of the left ventricle. The results of this study support the hypothesis of the relative voltage deficit in LVH. These results are consistent with the finding of a high number of false negative ECG results in clinical ECG diagnostics of LVH, and could contribute to an understanding of the diagnostic importance of the false negative ECG results, their re-evaluation and utilization for clinical diagnosis and prognosis.
  Clinical and Experimental Hypertension 08/2004; 26(6):557-67. · 1.07 Impact Factor
• Article: QRS voltage-duration product in the identification of left ventricular hypertrophy in spontaneously hypertensive rats.

  Ljuba Bacharova, Jan Kyselovic, Jan Klimas
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  ABSTRACT: Evaluation of the performance of the QRS voltage-duration product (VDP) for detection of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). Orthogonal electrocardiograms (ECG) were recorded in male SHR at the age of 12 and 20 weeks, when systolic blood pressure (sBP) reached the average values of 165+/-3 mmHg and 195+/-12 mmHg, respectively. Age- and sex- matched normotensive Wistar Kyoto (WKY) rats were used as controls. VDP was calculated as a product of maximum QRS spatial vector magnitude and QRS duration. Left ventricular mass (LVM) was weighed after rats were sacrificed. LVM in SHR at 12 and 20 weeks of age (0.86+/-0.05 g and 1.05+/-0.07 g, respectively) was significantly higher as compared with that in WKY (0.65+/-0.07 g and 0.70+/-0.02 g). The increase in LVM closely correlated with the sBP increase. VDP did not reflect the increase in LVM in SHR. VDP was lower in SHR as compared with that in WKY, and the difference was significant at the age of 20 weeks (18.2mVms compared with 10.7mVms, p<0.01). On the contrary, a significant increase in the VDP was observed in the control WKY at the age of 20 weeks without changes in LVM. The changes in VDP were influenced mainly by the changes in QRSmax. LVM was not the major determinant of QRS voltage changes and consequently of the VDP. These data point to the importance of the nonspatial determinants of the recorded QRS voltage in terms of the solid angle theory.
  Arquivos Brasileiros de Cardiologia 09/2002; 79(2):143-8. · 0.88 Impact Factor