RELATIVE CONTRIBUTIONS OF FIBROSIS AND CONNEXIN CHANGES TOTHE ATRIAL FIBRILLATION SUBSTRATE DURING THE DEVELOPMENT AND REVERSAL OF CONGESTIVEHEART FAILURE

2008 ◽  
Vol 31 (4) ◽  
pp. 5
Author(s):  
Brett Burstein ◽  
Kunihiro Nishida ◽  
Philippe Comtois ◽  
Louis Villenuve ◽  
Yung-Hsin Yeh ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potential Model ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Left Ventricular ◽  
Muscle Bundle ◽  
Protein Ratio ◽  
Conduction Disturbances ◽  
Conduction Abnormalities ◽  
Mrna And Protein Expression

Background: Connexin alterations occur in various atrial fibrillation (AF) paradigms, but their functional significance remains unclear. No data are available regarding the effects of CHF on atrial connexin expression and phosphorylation. We therefore analyzed connexin changes and their contribution to the AF substrate during the development and reversal ofCHF. Methods and Results: Dogs were allocated to three groups: CHF induced by 2-week ventricular tachypacing (CHF, n=15); CHF dogs allowed to recover for 4 weeks after 2-week tachypacing (REC, n=15) and non-paced shams (CTL, n=11). Left ventricular end-diastolic pressure increased with CHF (14.5±1.0*** vs.3.7±0.7, ***P < 0.001 vs. CTL) and normalized upon CHF recovery (5.1±1.0^†††, ^††† P < 0.001 vs. CHF). Real-time PCR and Western-blot analyses revealed connexin43 (Cx43) and connexin40 (Cx40) mRNA and protein expression to be unchanged by CHF and REC. However, CHF caused Cx43 dephosphorylation(by ~73%***) and increased Cx40/Cx43 protein ratio (by ~35%***), with both alterations completely reversing in REC. Immunofluorescent confocal microscopy confirmed connexin protein trends, with a reduction in phosphorylated Cx43 (by ~68%*** in CHF) that returned to control in REC. CHF caused conduction abnormalities (phasedelay-range and heterogeneity index, both P < 0.01) and burst pacing-induced AF prolongation (CTL 22±7s, CHF 1100±171s***, REC 884±220s***) which persisted in the recovery period, along with residual fibrosis (CTL 3.6±0.7%, CHF 14.7±1.5%***, REC13.3±2.3%***). Fibrosis physically interrupted muscle bundle continuity and anionically-based action potential model of canine atrium showed that fibrosiswas able to account for the observed conduction abnormalities. Conclusions: CHF causes connexin-dephosphorylation and Cx40/Cx43ratio increases. With CHF reversal, atrial connexin alterations recover completely, but tissue fibrosis, conduction abnormalities and a substrate forAF remain with fibrosis accounting for conduction abnormalities. Thus, althougha trial connexin changes occur with CHF, they are not essential for conduction disturbances and AF promotion, which appear rather to be related primarily tofibrotic interruption of muscle-bundle continuity.

scholarly journals Three Vessel Coronary Cameral Fistulae Associated with New Onset Atrial Fibrillation and Angina Pectoris

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Murat Yuksel ◽  
Abdulkadir Yildiz ◽  
Mustafa Oylumlu ◽  
Nihat Polat ◽  
Halit Acet ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Coronary Artery ◽  
Coronary Angiography ◽  
Left Ventricle ◽  
Coronary Arteries ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Ventricular Rate ◽  
Fistula Formation ◽  
New Onset

Coronary cameral fistulas are abnormal communications between a coronary artery and a heart chamber or a great vessel which are reported in less than 0.1% of patients undergoing diagnostic coronary angiography. All three major coronary arteries are even less frequently involved in fistula formation as it is the case in our patient. A 68-year-old woman was admitted to cardiology clinic with complaints of exertional dyspnea and angina for two years and a new onset palpitation. Standard 12-lead electrocardiogram revealed atrial fibrillation (AF) with a ventricular rate of 114 beat/minute and accompanying T wave abnormalities and minimal ST-depression on lateral derivations. Transthoracic echocardiographic examination was normal except for diastolic dysfunction, minimally mitral regurgitation, and mild to moderate enlargement of the left atrium. Sinus rhythm was achieved by medical cardioversion with amiodarone infusion. Coronary angiography revealed diffuse and multiple coronary-left ventricle fistulas originating from the distal segments of both left and right coronary arterial systems without any stenosis in epicardial coronary arteries. The patient’s symptoms resolved almost completely with medical therapy. High volume shunts via coronary artery to left ventricular microfistulas may lead to increased volume overload and subsequent increase in end-diastolic pressure of the left ventricle and may cause left atrial enlargement.

scholarly journals Atrial fibrillation modifies the association between pulmonary artery wedge pressure and left ventricular end-diastolic pressure

2017 ◽  
Vol 19 (11) ◽  
pp. 1483-1490 ◽  
Author(s):  
Michael G. Dickinson ◽  
Carolyn S. Lam ◽  
Michiel Rienstra ◽  
Ton E. Vonck ◽  
Yoran M. Hummel ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Pulmonary Artery ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Pulmonary Artery Wedge Pressure ◽  
Wedge Pressure

scholarly journals Heart Failure with Preserved Ejection Fraction – Concept, Pathophysiology, Diagnosis and Challenges for Treatment

2015 ◽  
Vol 3 (3) ◽  
pp. 521-527 ◽  
Author(s):  
Lidija Veterovska Miljkovik ◽  
Vera Spiroska
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Coronary Revascularization ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Elevated Concentration ◽  
Reduced Ejection Fraction

Heart failure (HF) with preserved left ventricular (LV) ejection fraction (HFpEF) occurs in 40 to 60% of the patients with HF, with a prognosis which is similar to HF with reduced ejection fraction (HFrEF). HFpEF pathophysiology is different from that of HFrEF, and has been characterized with diastolic dysfunction. Diastolic dysfunction has been defined with elevated left ventricular stiffness, prolonged iso-volumetric LV relaxation, slow LV filing and elevated LV end-diastolic pressure. Arterial hypertension occurs in majority cases with HFpEF worldwide. Patients are mostly older and obese. Diabetes mellitus and atrial fibrillation appear proportionally in a high frequency of patients with HFpEF. The HFpEF diagnosis is based on existence of symptoms and signs of heart failure, normal or approximately normal ejection and diagnosing of LV diastolic dysfunction by means of heart catheterization or Doppler echocardiography and/or elevated concentration of plasma natriuretic peptide. The present recommendations for HFpEF treatment include blood pressure control, heart chamber frequency control when atrial fibrillation exists, in some situations even coronary revascularization and an attempt for sinus rhythm reestablishment. Up to now, it is considered that no medication or a group of medications improve the survival of HFpEF patients. Due to these causes and the bad prognosis of the disorder, rigorous control is recommended of the previously mentioned precipitating factors for this disorder. This paper presents a universal review of the most important parameters which determine this disorder.

scholarly journals Altered E-C coupling in rat ventricular myocytes from failing hearts 6 wk after MI

2000 ◽  
Vol 279 (2) ◽  
pp. H798-H807 ◽  
Author(s):  
J. Andrew Wasserstrom ◽  
Even Holt ◽  
Ivar Sjaastad ◽  
Per Kristian Lunde ◽  
Annlaug Ødegaard ◽  
...  
Keyword(s):  
Left Coronary Artery ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Heart Weight ◽  
Channel Block ◽  
Voltage Range ◽  
Rat Hearts ◽  
Mrna And Protein Expression

Excitation-contraction (E-C) coupling was investigated in rat hearts 6 wk after induction of myocardial infarction (MI) by ligation of the left coronary artery. Heart weight was increased by 74% and left ventricular end-diastolic pressure was 23 ± 2 mmHg in MI compared with 8 ± 2 mmHg in sham-operated controls (Sham, P < 0.001). Cell shortening was measured in voltage-clamped myocytes at 36°C. In solutions where Cs+ had been replaced by K+, the voltage dependence of contraction was sigmoidal between −20 and +100 mV in Sham and MI cells. Verapamil (20 μM) blocked L-type Ca2+current and reduced contraction in Sham cells by ∼50% ( P < 0.01) but did not decrease contraction significantly in MI cells at test potentials above +10 mV. Verapamil-insensitive contractions were blocked by Ni2+ (5 mM). Na+/Ca2+ exchange current was doubled in MI compared with Sham cells at test potentials between −20 and +80 mV ( P < 0.05), whereas mRNA and protein expression increased by 30–40%. Finally, voltage dependence of contraction was bell shaped in Na+-free solutions, but contraction was significantly increased in MI cells over a wider voltage range ( P < 0.05). The insensitivity to Ca2+channel block in MI cells may result from an increased contribution of the Na+/Ca+ exchanger to triggering of E-C coupling. These results suggest significant changes in E-C coupling in the hypertrophy and failure that develop in response to extensive MI.

Antiarrhythmische Pharmakotherapie

2012 ◽  
Vol 31 (11) ◽  
pp. 826-829
Author(s):  
A. Goette ◽  
P. Kirchhof ◽  
A. Treszl ◽  
K. Wegscheider ◽  
T. Meinertz
Keyword(s):  
Atrial Fibrillation ◽  
Drug Therapy ◽  
Angiotensin Ii ◽  
Catheter Ablation ◽  
Early Treatment ◽  
Stroke Prevention ◽  
Conventional Treatment ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Atrial Fibrillation Trial

ZusammenfassungEs werden die Ergebnisse von Studien sowie die Protokolle laufender „Megastudien“ mit Bezug zum Vorhofflimmer-Netzwerk dargestellt. Bei den abgeschlossenen Studien handelt es sich um die Flecainide Short-Long trial (Flec-SL) und die Angiotensin-II-Rezeptorblocker in Paroxysmal Atrial FibrillationStudie (ANTIPAF). Bei den „Megastudien“ um Studien mit den Kürzeln EAST (Early Treatment of Atrial Fibrillation for Stroke Prevention Trial), CABANA (Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation Trial) und CASTLE-AF (Catheter Ablation versus Standard conventional Treatment in patients with LEft ventricular dysfunction and Atrial Fibrillation). Die Ergebnisse der Studien: Eine präventive Kurzzeittherapie nach Kardio-version ist sinnvoller als der Verzicht auf jegliche Antiarrhythmika-Nachbehandlung. Noch effektiver scheint eine antiarrhythmische Langzeit-Nachbehandlung über sechs Monate zu sein. In der ANTIPAF-Studie zeigte sich, dass bei Patienten mit paroxysmalem Vorhofflimmern (VHF) ohne strukturelle Herzkrankheit der Angiotensinrezeptorblocker Olmesartan nicht in der Lage ist, die Häufigkeit der Anfälle zu reduzieren. Wichtigstes therapeutisches Ziel ist die Verhinderung der Progression von VHF. In der EAST-Studie wird geprüft, ob eine frühzeitig eingeleitete, „aggressive“ Therapie zur Kontrolle des Herzrhythmus eher in der Lage ist, Morbidität und Mortalität von VHF zu senken als die Standardtherapie.

Acute Changes in Left Ventricular End Diastolic Pressure following the Transcatheter Closure of an Atrial Septal Defect in Adults

2016 ◽  
Vol 19 (3) ◽  
pp. 145 ◽  
Author(s):  
Young Hwa Kong ◽  
Jinyoung Song ◽  
Kyung Hee Kim ◽  
June Huh ◽  
I-Seok Kang
Keyword(s):  
Elderly Patients ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Transcatheter Closure ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Device Closure ◽  
Acute Changes ◽  
Asd Closure

<strong>Background:</strong> Acute changes in left ventricular diastolic function shortly after ASD closure in elderly patients have not been well known. We aimed to investigate acute changes in left ventricular end diastolic pressure (LVEDP) in elderly patients following transcatheter closure of atrial septal defect (ASD). <br /><strong>Methods:</strong> All 19 adults with ASDs who underwent transcatheter closure between June 2013 and December 2014 were enrolled. LVEDP was measured prior to device closure and compared with that immediately following device closure and 15 minutes after device closure. <br /><strong>Results:</strong> The median age of the patients was 48 years old. The baseline E/e’ and LVEDP values were 8.3 ± 2.8 and 13 ± 3 mmHg. The LVEDP value immediately following closure was 19 ± 4 mmHg, and 15 minutes after closure was 16 ± 4 mmHg. The median increase in the LVEDP value immediately following closure was 6 mmHg, which significantly differed from that prior to closure. The LVEDP 15 minutes after closure decreased but remained significantly higher than the value observed immediately after closure. No significant changes were observed with regard to E/e’ at either 1 day or 3 months following closure. The LVEDP value <br />15 minutes after device closure was significantly correlated with those observed before closure and immediately following closure; however, no significant correlations were observed with regard to patient age, Qp/Qs, E/e’ before closure, or E/e’ 3 months after device closure.<br /><strong>Conclusion:</strong> LVEDP in adults with ASDs significantly increases following device closure. LVEDP before closure predicts LVEDP following device closure.

Sign in / Sign up

Export Citation Format

Share Document