scholarly journals Carvedilol and Pycnogenol® improve the function of diabetic hearts in rats

2013 ◽  
Vol 60 (2) ◽  
pp. 15-21
Author(s):  
Kráľová E. ◽  
Jankyová S. ◽  
Pekárik A. ◽  
Čuboň J. ◽  
Stankovičová T.
Keyword(s):  
Blood Pressure ◽  
Electrical Activity ◽  
Qt Interval ◽  
Heart Function ◽  
Left Ventricular ◽  
Biometric Parameters ◽  
Haemodynamic Parameters ◽  
Arterial Blood ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

Abstract We observed the changes in electrical activity, biometric and haemodynamic parameters of hearts in animals with experimental diabetes mellitus (DM). As well the effect of carvedilol, PycnogenolR and its combination with carvedilol on DM heart function was tested. DM was induced by streptozotocin over three sequential days at a dose of 25 mg/kg body weight i.p. We started therapy by suspension of carvedilol, PycnogenolR and their combination for six weeks. Blood pressure was measured using tail cuff plethysmography. ECG, haemodynamic and biometric parameters were measured in isolated hearts perfused according to the Langendorff. DM rats had increased systolic arterial blood pressure, thicker free wall of left ventricle but weakened myocardial contractility compared with controls. In contrast to controls, electrophysiological parameters showed prolonged QT interval and increased incidence of dysrhythmias in DM rats. The PycnogenolR administration induced regression of left ventricular hypertrophy, improved left ventriculi contraction and increased coronary flow; however, it did not improve the electrical activity of the myocardium compared with DM ones. Carvedilol also reversed the myocardial remodelling, shortened the duration of QT interval and suppressed the incidence of dysrhythmias. The common combination of drugs improved biometric and haemodynamic parameters compared with DM animals, however, not so significantly as monotherapy. On the other hand, the combination of carvedilol and PycnogenolR significantly reduced the duration of the QT interval and shortened the incidence of dysrhythmias. We can conclude that the administration of PycnogenolR effectively improved haemodynamic parameters, and carvedilol affected biometric parameters and also electrical parameters in DM animals. We observed the marked synergic effect of the combination of both drugs on the electrical activity of myocardium. This combination shortened the most pathologically prolonged QT interval and reduced the number of dysrhythmias.

Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia

2010 ◽  
Vol 299 (3) ◽  
pp. G784-G790 ◽  
Author(s):  
Søren Møller ◽  
Jens S. Iversen ◽  
Aleksander Krag ◽  
Peter Bie ◽  
Andreas Kjær ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Qt Interval ◽  
Baroreflex Sensitivity ◽  
Arterial Oxygen ◽  
Pulmonary Dysfunction ◽  
Oxygen Inhalation ◽  
Arterial Blood ◽  
Cirrhotic Patients ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (DlCO), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (PaO2) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 ± 0.8 vs. 10.3 ± 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients ( P < 0.05). There was no significant difference in BRS according to presence of HPS, PaO2, DlCO, or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.

scholarly journals A Case of Thiazide-induced Hypokalemic Paralysis

2019 ◽  
Vol 3 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Elizabeth Schell ◽  
Joshua Pathman ◽  
Richard Pescatore ◽  
Pollianne Bianchi
Keyword(s):  
Blood Pressure ◽  
Alcohol Abuse ◽  
Qt Interval ◽  
Periodic Paralysis ◽  
Elevated Blood ◽  
Magnesium Supplementation ◽  
T Wave ◽  
St Depression ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

We describe the case of a patient presenting with odd neurologic symptoms initially thought to represent somatization who was found to have critical hypokalemia manifesting as hypokalemic non-periodic paralysis. It was determined that the patient had baseline hypokalemia as a function of alcohol abuse, exacerbated by self overmedication with hydrochlorothiazide for elevated blood pressure readings at home. The diagnosis was suspected when an electrocardiogram was obtained demonstrating a pseudo-prolonged QT interval with ST depression, consistent with T-U wave fusion and a QU interval with an absent T wave.1 The patient received oral and intravenous potassium and magnesium supplementation with resolution of symptoms.

Wide Complex Tachycardia

2016 ◽  
Author(s):  
Gary Green ◽  
Sally Graglia
Keyword(s):  
Ventricular Tachycardia ◽  
Qt Interval ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Qt Prolongation ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Wpw Syndrome ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

Wide-complex tachycardias (WCTs) should always alert the emergency physician to a potentially immediate or rapidly developing, life-threatening scenario. The approach to these patients should follow general emergency medicine principles. The review covers the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of WCT. Figures show a basic electrocardiogram (ECG) tracing, an ambulatory monitoring strip of a patient with recurrent presyncope showing repetitive monomorphic ventricular tachycardia, a 12-lead ECG of a rapid wide QRS tachycardia due to an antidromic atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White (WPW) syndrome, an example of pacemaker-mediated tachycardia, ventricular tachycardia occurring in the context of QT prolongation consistent with torsades de pointes, a 12-lead ECG in a patient with WPW syndrome showing a rapid, irregular ventricular rate and wide QRS complexes of atrial fibrillation with a short refractory period, an ECG representative of tricyclic antidepressant overdose, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection fraction less than or equal to 35% who are candidates for an implantable cardioverter-defibrillator. Tables list causes of regular WCT, causes of prolonged QT interval, common medications with potential QT prolongation activity, pharmacologic treatment options for stable patients with WCT, Kindwall and colleagues’ criteria for ventricular tachycardia, Brugada and colleagues’ criteria for ventricular tachycardia, Vereckei and colleagues’ aVr algorithm for the diagnosis of ventricular tachycardia, and a comparison of self-reported sensitivities, specificities, and test accuracies of the algorithms presented by Kindwall, Brugada, and Vereckei and their colleagues.   Key words: prolonged QT interval, supraventricular tachycardia, ventricular tachycardia, wide-complex tachycardias   This review contains 8 highly rendered figures, 8 tables, and 59 references.

scholarly journals Prevalence of Abnormal and Borderline Electrocardiogram Changes in 13, 079 Chinese Amateur Marathon Runners

2020 ◽  
Author(s):  
Xu Wen ◽  
Yumin Huang ◽  
Tonghui Shen ◽  
Yinglan Gong ◽  
Ruiqing Dong ◽  
...  
Keyword(s):  
Qt Interval ◽  
Sinus Bradycardia ◽  
Premature Ventricular Contraction ◽  
Left Ventricular ◽  
Ecg Changes ◽  
Sinus Arrhythmia ◽  
Marathon Runners ◽  
St Segment ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

Abstract The purpose of this study was to assess the prevalence of normal, borderline and abnormal ECG changes in marathon runners. The 12-lead ECG data of 13,079 amateur marathon runners between the ages of 18 and 35 years were included for analysis. The prevalence of ECG abnormalities among different gender groups was compared with chi-square tests. In terms of training-related changes, sinus bradycardia, sinus arrhythmia and left ventricular high voltage were found in approximately 15%, 5% and 3.28% of the participants, respectively. The incidence of right axis deviation in the marathon runners was 1.78%, which was slightly higher than the incidence of left axis deviation (0.88%). No more than 0.1% of the amateur marathon runners exhibited ST segment depression, T wave inversion (TWI), premature ventricular contraction, pathologic Q waves and prolonged QT interval. In conclusion, training-related ECG changes, including sinus bradycardia, sinus arrhythmia and left ventricular high voltage, were common in the amateur marathon runners. Most of abnormal ECG changes, including ST segment depression, TWI, premature ventricular contraction, pathologic Q waves and prolonged QT interval, were infrequently found in the amateur marathon runners.

Prolonged QT interval during diabetic ketoacidosis: A case series

2020 ◽  
Author(s):  
Ghariani Rania ◽  
Chrif Yosra ◽  
Samar Derbal ◽  
Rihab Laamouri ◽  
Fatma Ben Dahmene ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Qt Interval ◽  
Case Series ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

scholarly journals Changes in left ventricular electromechanical relations during targeted hypothermia

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Kristin Wisløff-Aase ◽  
Viesturs Kerans ◽  
Kristina Haugaa ◽  
Per Steinar Halvorsen ◽  
Helge Skulstad ◽  
...  
Keyword(s):  
Heart Rate ◽  
Qt Interval ◽  
Clinical Importance ◽  
Left Ventricular ◽  
Peak Strain ◽  
Time To Peak ◽  
Mechanical Dispersion ◽  
Dispersion Of Repolarization ◽  
Aortic Valve Closure ◽  
Prolonged Qt Interval

Abstract Background Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion. Methods In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (− 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (− 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297). Conclusion Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.

scholarly journals Association arterial stiffness reduction with improved left ventricular longitudinal and torsional deformation after 3 years of antihypertensive treatment

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Tzortzis ◽  
I Ikonomidis ◽  
H Triantafyllidi ◽  
J Thymis ◽  
A Frogoudaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Ace Inhibitors ◽  
Antihypertensive Treatment ◽  
Left Ventricular ◽  
Torsional Deformation ◽  
Flow Reserve ◽  
Stiffness Reduction ◽  
Arterial Blood ◽  
Lv Mass

Abstract Background We investigated the effects of antihypertensive treatment on vascular function, longitudinal and torsional deformation in hypertensives. Methods In 200 untreated patients with arterial hypertension (age 52.5±11.6 years, 56% females), we measured at baseline and after a 3-year of antihypertensive treatment (160 received ACEi± diuretics and 40 CCBs± diuretics): a) 24h ambulatory blood pressure b) Carotid-femoral pulse wave velocity (PWV) b) Coronary flow reserve (CFR), LV mass index (LVMI), the global longitudinal strain (GLS) and diastolic (LongSRSE) strain rate, peak twisting (Tw-deg) and untwisting at mitral valve opening (UtwMVO), at peak E (UtwE) and at the end of the E wave (UtwendE) of the mitral inflow as well as twisting (TwVel-deg/sec) velocity using speckle tracking imaging. We calculated the % change of LV untwisting as difference between peakTw and UtwMVO, UtwpeakE and UtwendE. Results Compared to baseline, there was an improvement of GLS (−19.9±3.4 vs. −18.7±3.1%), LongSRS (−1.08±0.22 vs. −0.98±0.26 1/s), LongSRE (1.09±0.36 vs. 0.99±0.31 1/s), peak Tw (16.2±5.1 vs. 18.7±5.9 deg), Tw velocity, and the %LV untwisting (31.04±19.28 vs 26.02±15.69% at MVO, 60.04±19.78 vs 53.96±19.76% at peakE and 79.98±14.24 vs 75.90±17.01% at endE) post-treatment. In parallel, CFR (2.72±0.61 vs. 2.55±0.64), PWV (10.34±1.93 vs. 11.2±2.08 m/s) and LVMI were improved (p&lt;0.01 for all comparisons). By ANOVA, the interaction term between changes of all the above parameters and antihypertensive treatment (ACE inhibitors vs calcium channel blockers) was not significant (p&gt;0.05). By multivariate analysis, the reduction of 24h meanBP and PWV independently determined the respective improvement of GLS (b=0.478 and b=0.248 respectively), LongS (b=0.428 and b=0.201 respectively) as well as Twisting (b=0.449 and b=0.294 respectively) after adjusting for changes in LV mass, CFR and atherosclerotic risk factors (p&lt;0.05). Conclusions Long-term optimal blood pressure control with ACE inhibitors and CCBs improves LV longitudinal and torsional mechanics in hypertensives in parallel with arterial stiffness and blood pressure. This improvement in LV deformation and twisting was independently related to changes in arterial blood pressure and arterial stiffness. Funding Acknowledgement Type of funding source: None

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

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