P6655The impact of paced QRS duration on the expression of genes related to contractile function and hypertrophy of the left ventricle in chronically paced patients from the right ventricular apex

Abstract Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in reduced extravascular compressive forces and myocardial oxygen demand. Right ventricular perfusion has eight major characteristics that distinguish it from left ventricular perfusion: (1) appreciable perfusion throughout the entire cardiac cycle; (2) reduced myocardial oxygen uptake, blood flow, and oxygen extraction; (3) an oxygen extraction reserve that can be recruited to at least partially offset a reduction in coronary blood flow; (4) less effective pressure–flow autoregulation; (5) the ability to downregulate its metabolic demand during coronary hypoperfusion and thereby maintain contractile function and energy stores; (6) a transmurally uniform reduction in myocardial perfusion in the presence of a hemodynamically significant epicardial coronary stenosis; (7) extensive collateral connections from the left coronary circulation; and (8) possible retrograde perfusion from the right ventricular cavity through the Thebesian veins. These differences promote the maintenance of right ventricular oxygen supply–demand balance and provide relative resistance to ischemia-induced contractile dysfunction and infarction, but they may be compromised during acute or chronic increases in right ventricle afterload resulting from pulmonary arterial hypertension. Contractile function of the thin-walled right ventricle is exquisitely sensitive to afterload. Acute increases in pulmonary arterial pressure reduce right ventricular stroke volume and, if sufficiently large and prolonged, result in right ventricular failure. Right ventricular ischemia plays a prominent role in these effects. The risk of right ventricular ischemia is also heightened during chronic elevations in right ventricular afterload because microvascular growth fails to match myocyte hypertrophy and because microvascular dysfunction is present. The right coronary circulation is more sensitive than the left to α-adrenergic–mediated constriction, which may contribute to its greater propensity for coronary vasospasm. This characteristic of the right coronary circulation may increase its vulnerability to coronary vasoconstriction and impaired right ventricular perfusion during administration of α-adrenergic receptor agonists.

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Developments in Conventional Pacing – Harmful Effects of Pacing the Right Ventricular Apex and Strategies to Avoid it

European Cardiology Review ◽

10.15420/ecr.2006.0.2.1g ◽

2006 ◽

Vol 0 (2) ◽

pp. 1

Author(s):

Mark C S Hall ◽

Johan E P Waktare ◽

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Keyword(s):

Right Ventricular ◽

Right Ventricular Apex ◽

The Right ◽

Harmful Effects

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CONDITION OF HEMODYNAMICS IN THE PULMONARY CIRCULATION OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CONCURRENT WITH METABOLIC SYNDROME WITH HYPERTROPHY AND ATROPHY OF THE MYOCARDIUM

Wiadomości Lekarskie ◽

10.36740/wlek201908114 ◽

2019 ◽

Vol 72 (8) ◽

pp. 1491-1493

Author(s):

Viktor P. Boriak ◽

Svitlana V. Shut’ ◽

Tetiana A. Trybrat ◽

Olena V. Filatova

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Metabolic Syndrome ◽

Right Ventricular ◽

Pulmonary Disease ◽

Pulmonary Circulation ◽

Contractile Function ◽

Ventricular Myocardium ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

The Right

Introduction: In recent years, COPD is observed as not an isolated, but an associated pathology, in particular, concurrent with metabolic syndrome. The aim of the research is to identify the differences in changes of the rheopulmonography parameters (RPG) depending on the presence of hypertrophy or atrophy of the right ventricular myocardium in patients with COPD concurrent with metabolic syndrome.. Materials and methods: We studied changes in rheopulmonography (RPG) in 145 patients with chronic obstructive pulmonary disease (COPD) concurrent with metabolic syndrome. Results: We detected precapillary hypertension of the pulmonary circulation in patients with right ventricular myocardial hypertrophy: anacrotism serration; flattened peak of the systolic wave; decreased Vcp; high placement of incisura; horizontal course of catacrotism; decreased amplitude of the systolic wave (in this case, due to a greater increase in the resistance of the blood flow in the pulmonary vessels than the decreased impact volume of the right ventricle); prolonged Q-a (in this group of patients, it depends more on hypertension of the pulmonary circulation than on the reduction of contractile function of the myocardium). In atrophy of the right ventricular myocardium, the following changes in the RPG were revealed: decreased systolic wave at its dramatic rise; prolonged Q-a (in this case, due to the weakened heart contraction); Vmax reduction (it reflects the reduction of myocardial contractility); in hypertrophy of the myocardium, Vcp., unlike RPG, does not decrease, which is explained by the decrease in the pressure of the pulmonary circulation. Conclusions: We believe that these changes in RPG allow differentiating hypertrophy and right ventricular myocardial atrophy along with established diagnostic criteria, and can be used as markers for the diagnosis and treatment of COPD concurrent with metabolic syndrome.

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Idiopathic ventricular tachycardia arising from the right ventricular apex

EP Europace ◽

10.1093/europace/eun239 ◽

2008 ◽

Vol 10 (11) ◽

pp. 1343-1345 ◽

Cited By ~ 5

Author(s):

A. Navarrete

Keyword(s):

Ventricular Tachycardia ◽

Right Ventricular ◽

Idiopathic Ventricular Tachycardia ◽

Right Ventricular Apex ◽

The Right

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Recurrent appearance of protective zones after an unsuccessful defibrillation shock

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.4.h1491 ◽

1996 ◽

Vol 271 (4) ◽

pp. H1491-H1497 ◽

Cited By ~ 1

Author(s):

C. Hwang ◽

W. Fan ◽

P. S. Chen

Keyword(s):

Right Ventricular ◽

Energy Requirement ◽

Right Ventricular Outflow Tract ◽

Posterior Wall ◽

Ventricular Outflow Tract ◽

Specific Time ◽

Time Intervals ◽

Cycle Lengths ◽

Right Ventricular Apex ◽

The Right

This study was designed to test the hypothesis that protective zones appear recurrently at the initiation of ventricular fibrillation (VF) and that when shocks are delivered during protective zones, there can be a decrease in the defibrillation energy requirement. A total of 12 open-chest dogs were studied. Six dogs were included in protocol 1. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. In protocol 2, we delivered unsuccessful defibrillation shocks via a transvenous defibrillation electrode placed in the right ventricular apex of six dogs. A second shock was then delivered to patch electrodes on the right ventricular outflow tract and the posterior wall of the left ventricle. The results of protocol 1 showed that the S3 terminated reentry and prevented VF only when it occurred at specific time intervals after the S2 (the protective zones). These protective zones appear recurrently up to 375 ms after the onset of VF. The results of protocol 2 showed that the total energy required for successful defibrillation was dependent on the interval between the first and second shocks. Intervals favoring effective defibrillation (protective zones) appeared recurrently for up to 280 ms after the first shock. When the second shock was delivered during a protective zone, the defibrillation energy requirement was decreased by up to 23% (from 13.1 +/- 2.0 to 10.1 +/- 1.8 J, P < 0.003). However, when the shock was delivered outside the protective zone, a significant increase in the defibrillation energy requirement was observed. We conclude that protective zones appear recurrently at the onset of VF and after unsuccessful defibrillation shocks.

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Failure of Cellularization of Ventriculotomy Patch Leading to Right Ventricular Pseudoaneurysm

World Journal for Pediatric and Congenital Heart Surgery ◽

10.1177/2150135119880547 ◽

2019 ◽

Vol 11 (1) ◽

pp. 123-126

Author(s):

Sruti Rao ◽

Robert D. Stewart ◽

Gosta Pettersson ◽

Carmela Tan ◽

Suzanne Golz ◽

...

Keyword(s):

Left Ventricle ◽

Ventricular Septal Defect ◽

Right Ventricle ◽

Right Ventricular ◽

Septal Defect ◽

Tricuspid Atresia ◽

Outflow Obstruction ◽

Ventricular Outflow Obstruction ◽

The Right ◽

Double Inlet Left Ventricle

Enlargement of the bulboventricular foramen (BVF) in double-inlet left ventricle or the ventricular septal defect (VSD) in tricuspid atresia with transposition of the great arteries is one approach for prevention or treatment of systemic ventricular outflow obstruction. Most often, BVF/VSD restriction is bypassed preemptively or addressed directly at the time of Glenn/Fontan procedures as part of staged univentricular palliation. We describe a patient who underwent enlargement of a restrictive VSD during Fontan completion and subsequently presented with an asymptomatic pseudoaneurysm of the right ventricle at the ventriculotomy site.

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