Successful cryoablation of left ventricular summit premature ventricular contractions via the coronary sinus

2020 ◽  
Vol 43 (8) ◽  
pp. 894-897
Author(s):  
William Reichert ◽  
Zeshan Ahmad ◽  
Wilber Su
Keyword(s):  
Coronary Sinus ◽  
Left Ventricular ◽  
Premature Ventricular Contractions

Dilated coronary sinus mimicking posterior left ventricular aneurysm

2001 ◽  
Vol 56 (3) ◽  
pp. 199-200 ◽  
Author(s):  
Theodor TIRILOMIS ◽  
Federico L. SALDAÑA ◽  
Harald DALICHAU
Keyword(s):  
Coronary Sinus ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Ventricular Aneurysm ◽  
Dilated Coronary Sinus

Effects of Elevated Coronary Sinus Pressure on Coronary Blood Flow and Left Ventricular Function

Circulation ◽  
1995 ◽  
Vol 92 (9) ◽  
pp. 298-303 ◽  
Author(s):  
Takuya Miura ◽  
Takeshi Hiramatsu ◽  
Joseph M. Forbess ◽  
John E. Mayer
Keyword(s):  
Blood Flow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Left Ventricular ◽  
Sinus Pressure

scholarly journals A case report: percutaneous management of high-output heart failure from iatrogenic aortocoronary venous grafting to the coronary sinus

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Akarsh Parekh ◽  
Vivek Sengupta ◽  
Ryan Malek ◽  
Mark Zainea
Keyword(s):  
Heart Failure ◽  
Coronary Sinus ◽  
Saphenous Vein Graft ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Covered Stents ◽  
Bypass Grafting ◽  
Output State ◽  
State Management ◽  
High Output

Abstract Background Aortocoronary arteriovenous fistula (ACAVF) due to iatrogenic bypass grafting to a cardiac vein is an exceedingly rare complication resulting from coronary artery bypass grafting (CABG) surgery. If not identified in a timely fashion, ACAVF has known significant clinical consequences related to left to right shunting and possible residual myocardial ischemia. Case presentation An 82-year-old male with a history of CABG, presented with dyspnea. Over the span of 2 years following CABG, the patient experienced progressive exertional dyspnea and peripheral edema. The patient was found to have a new cardiomyopathy with a severely reduced ejection fraction at 30–35%. The patient underwent diagnostic left heart catheterization, and an ACAVF was discovered between a saphenous vein graft and the coronary sinus. The patient underwent successful percutaneous coiling of the ACAVF with no residual flow. Follow-up echocardiography at 3 months revealed restoration of left ventricular systolic function to 50% and significant improvement in heart failure symptoms. Conclusions ACAVF is an exceedingly rare iatrogenic complication of CABG that may result in residual ischemia from the non-grafted myocardial territory and other sequelae relating to left to right shunting and a high-output state. Management for this pathology includes but is not limited to the use of percutaneous coiling, implantation of covered stents, graft removal and regrafting, and ligation.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Basic determinants of epicardial transudation

1997 ◽  
Vol 273 (3) ◽  
pp. H1408-H1414 ◽  
Author(s):  
R. H. Stewart ◽  
D. A. Rohn ◽  
S. J. Allen ◽  
G. A. Laine
Keyword(s):  
Reflection Coefficient ◽  
Coronary Sinus ◽  
Myocardial Edema ◽  
Hydraulic Conductance ◽  
Linear Increase ◽  
Left Ventricular ◽  
Edema Formation ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Osmotic Reflection Coefficient

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

Abstract P170: Nicorandil Inhibits Gáq-Induced Chronic Heart Failure in Transgenic Mice

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Masamichi Hirose ◽  
Yasuchika Takeishi ◽  
Hisashi Shimojo ◽  
Toshihide Kashihara ◽  
Tsutomu Nakada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transgenic Mice ◽  
Structural Changes ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Acute Administration ◽  
Sulfonylurea Receptor ◽  
Inhibitory Effects ◽  
Premature Ventricular Contractions ◽  
Beneficial Effects

Introduction: Beneficial effects of nicorandil on the treatment of hypertensive heart failure (HF) and ischemic heart disease have been suggested. However, whether nicorandil has inhibitory effects on HF and ventricular arrhythmias caused by the activation of G protein alpha q (Gαq) -coupled receptor (GPCR) signaling pathway still remains unknown. We examined effects of chronic and acute administration of nicorandil on the development of HF and ventricular action potential (VAP) in transgenic mice with transient cardiac expression of activated Gαq (Gαq-TG), respectively. Method and Results: Nicorandil (6 mg/kg/day) or vehicle was chronically administered in Gαq-TG mice for 24 weeks from 8 weeks of age, and then ventricular function, and electrical and structural changes were investigated in the hearts. Chronic nicorandil administration improved the reduction of left ventricular fractional shortening (p < 0.001) in Gαq-TG hearts. During 10 min of electrocardiogram recording, premature ventricular contractions (more than 20 beats/min) were observed in 7 of 10 vehicle-treated Gαq-TG but in none of 10 nicorandil-treated Gαq-TG hearts (p < 0.01). QT interval was significantly shorter in nicorandil-treated Gαq-TG than in vehicle-treated Gαq-TG hearts (p < 0.05). Chronic nicorandil administration improved the increased ventricular interstitial fibrosis (p < 0.05) but not cardiac hypertrophy in Gαq-TG left ventricles. Real time RT-PCR revealed that mRNA expression levels of s sulfonylurea receptor 2B (SUR-2B) were decreased in vehicle-treatd Gαq-TG but not in nicorandil-treated Gαq-TG. In addition, chronic nicorandil increased endotherial nitric oxide syntheses gene expression in Gαq-TG hearts (p < 0.05). Acute nicorandil administration (1 microM) significantly shortened the prolonged VAP duration and reduced the number of PVCs in vehicle treated Gαq-TG hearts. Conclusions: These findings suggest that nicorandil inhibits ventricular electrical and structural remodeling and arrhythmias through the shortening of VAP duration and the increased expression of SUR-2B and eNOS in a mouse model of HF.

MANAGEMENT OF HEART FAILURE PATIENTS (UPDATE 2019) – PHARMACOLOGICAL THERAPY

2020 ◽  
Vol 1 (54) ◽  
pp. 30-32
Author(s):  
Przemysław Mitkowski ◽  
Maciej Grymuza
Keyword(s):  
Heart Failure ◽  
Biventricular Pacing ◽  
Total Mortality ◽  
Cardiovascular Death ◽  
Left Ventricular ◽  
Pharmacological Therapy ◽  
Left Ventricular Ejection ◽  
Premature Ventricular Contractions ◽  
Ventricular Ejection Fraction ◽  
Patients With Heart Failure

The up-date of ESC Guidelines on the management of patients with heart failure was published last year. The beneficial effect of a new group of drugs (flozins, sacubitril/valsartan - ARNI) in patients with heart failure was pointed out. These drugs not only prevent the onset of heart failure but also reduce HF hospitalization rate and in patients with reduced left ventricular ejection fraction decrease risk of cardiovascular death and in case of empagliflozin, dapagliflozin or sacubitril/valsartan also total mortality. These latter medicines reduce also the likelihood of sudden cardiac death. ARNI reduce the number of appropriate ICD shocks, the incidence of non-sustained VT, premature ventricular contractions, and increase percentage of biventricular pacing in car­diac resynchronization recipients.

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