US ‐guided vascular access and left ventricular rapid pacing in TAVR : Two simple points that may improve patients' outcomes

2020 ◽  
Vol 96 (2) ◽  
pp. 440-441
Author(s):  
Giuseppe Musumeci ◽  
Stefano Albani
Keyword(s):  
Vascular Access ◽  
Left Ventricular ◽  
Rapid Pacing ◽  
Simple Points

Positive inotropism in hypothermia partially depends on an increase in maximal Ca(2+)-activated force

1991 ◽  
Vol 261 (4) ◽  
pp. H1005-H1010 ◽  
Author(s):  
H. Kusuoka ◽  
Y. Ikoma ◽  
S. Futaki ◽  
H. Suga ◽  
A. Kitabatake ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Oxygen Consumption ◽  
Mild Hypothermia ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Phosphorus Compounds ◽  
Resonance Spectroscopy ◽  
Positive Inotropism ◽  
Rapid Pacing ◽  
Intact Heart

We investigated the contribution of maximal Ca(2+)-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca(2+)-activated pressure (MCAP), the intact-heart correlate of maximal Ca(2+)-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca2+ concentrations greater than or equal to 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 +/- 0.28% (mean +/- SE, P less than 0.001, n = 19) for each degree of myocardial cooling between 30 and 38 degrees C. Our results indicate that a primary change in myofilament Ca2+ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca(2+)-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.

scholarly journals P1296CARDIAC COMPLICATIONS OF ARTERIOVENOUS FISTULAS IN PATIENTS WITH END-STAGE RENAL DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Nessrine Breik ◽  
Hela Jbeli ◽  
Safa Fattoum ◽  
Imen Ouertani ◽  
Badreddine Ben kaab ◽  
...  
Keyword(s):  
Vascular Access ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Chronic Hemodialysis ◽  
Cardiac Complications ◽  
Arteriovenous Fistulas ◽  
Coronary Syndrome ◽  
Group 2 ◽  
Stage Renal Disease ◽  
Cardiac Status

Abstract Background and Aims Current literature suggests the arteriovenous fistula (AVF) to be the preferred type of vascular access for hemodialysis. However, AVFs have significant and potentially deleterious effects on cardiac functions particularly in the setting of preexisting heart disease. The aim of this study is to compare the clinical and echocardiographic evolution after creation of a proximal AVF and a radial AVF. Method We conducted a retrospective descriptive study including all chronic hemodialysis patients through AVF. Group 1 (G1) included patients with proximal AVF and group 2 (G2) patients with radial AVF. Results Twenty-four patients were collected in G1 and the average age was 55 years. G2 included 13 patients with a mean age of 44 years. Systolic blood pressure decreased after AVF creation in both groups (G1: 62.5%, G2: 45%, NS). A dyspnea was noted in 70% of cases of G1 and 38.4% of cases of G2 (NS). The interventricular septum was thickened in 20.8% of cases of G1 and 38.4% of G2 (NS). Left ventricular (LV) dilatation was observed in both groups with LV diastolic telegram diameter increase of 58% in G1 versus 10% in G2 (p = 0.04). A decrease in LV ejection fraction was found in 62.5% in G1 and 46.1% in G2 (p = 0.066). The major cardiac complications in G1 were acute coronary syndrome in 5 patients and atrial fibrillation in 4 cases after an average of 60 months and 35 months, respectively. No cardiac complications were noted in G2. Conclusion AVFs remain the preferred type of vascular access for chronic hemodialysis therapy because they are associated with better long-term patency and fewer complications compared with synthetic grafts. Its seat will depend on the vascular state and the cardiac status of the dialysis patient.

Abstract 565: The Activation of AMP-Activated Protein Kinase Ameliorates the Severity of Heart Failure in Dogs

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hideyuki Sasaki ◽  
Hiroshi Asanuma ◽  
Masashi Fujita ◽  
Hiroyuki Takahama ◽  
Masakatsu Wakeno ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase ◽  
Cardiac Myocytes ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Cellular Damage ◽  
Control Group ◽  
Compound C ◽  
Rapid Pacing ◽  
Amp Activated Protein Kinase

Backgrounds; Since AMP-activated protein kinase (AMPK) is activated in the pressure-overloaded hypertrophic hearts, we investigated whether the activation of AMPK caused by metformin attenuates the progression of heart failure induced by rapid pacing in dogs and decreases cellular damage caused by oxidative stress in neonatal rat cardiac myocytes. Methods and Results; Heart failure was induced by right ventricular (RV) pacing at 230 bpm for 4 weeks in dogs. Treatment of dogs with metformin (100mg/kg/day, orally, n=8, Met group) for 4 weeks prevented significantly the progression of pacing-induced heart failure evaluated by echocardiographical and hemodynamic measurement compared with the control group (n=8). Left ventricular (LV) diastolic and systolic dimension (LVDd and LVDs) were smaller (32.8±0.4 and 26.7±0.9 mm, respectively) and fractional shortening (FS) and ejection fraction (EF) were preserved in Met group (18.6±1.8 and 45.5±3.5 %, respectively) compared with the control group (LVDd and LVDs; 36.5±1.0 and 33.0±1.0 mm, FS and EF; 9.6±0.7 and 27.0±1.9 %, p<0.05 vs. Met group each). Furthermore, both pulmonary capillary wedge pressure (PCWP) and mean pulmonary arterial pressure (mPA) were significantly lower in Met group (11.1±0.9 and 18.1±1.4 mmHg, respectively) compared with the control group (21.0±2.2 and 26.8±2.8 mmHg, respectively). Treatment of cultured cardiac myocytes with a maximal physiological concentration of metformin (10μmol/L) attenuated the cellular damage against H 2 O 2 exposure (50μmol/L). These effects were blunted by an AMPK inhibitor, compound-C (20μmol/L), suggesting that the activation of AMPK increased the cellular viability during H 2 O 2 exposure. Conclusions; Metformin that activates AMPK prevented the progression of heart failure induced by rapid pacing in dogs and attenuated the cellular damage against H 2 O 2 exposure in cardiac myocytes. AMPK may be one of new targets for preventing heart failure in clinical settings.

P6484Invasive and non-invasive characterisation of low gradient aortic stenosis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Z R McConkey ◽  
M Marber ◽  
J Lee ◽  
H Ellis ◽  
J Joseph ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Research Training ◽  
Augmentation Index ◽  
Myocardial Perfusion Reserve ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Stress Perfusion ◽  
Stroke Work ◽  
Rapid Pacing

Abstract Background Low gradient severe aortic stenosis (LGAS) is associated with unfavourable outcomes when compared to high gradient aortic stenosis (HGAS), yet the contributing pathophysiology is poorly understood. Methods Symptomatic LGAS and HGAS patients undergoing trans-catheter aortic valve implantation (TAVI) underwent 3T stress perfusion cardiac magnetic resonance imaging (CMR) pre-(within 24 hours) and post-(4–6 months) TAVI. Left ventricular (LV) contractility and coronary flow/pressure were measured during hyperaemia and rapid pacing, immediately before and after TAVI, using a conductance LV catheter and dual-pressure and Doppler sensor–tipped guidewire in the mid-left anterior descending coronary artery. Results 24 patients were recruited resulting in 19 suitable datasets (LGAS N=9, HGAS N=10, equally matched for comorbidities and B-natriuretic peptide level). LGAS patients had a smaller LV end diastolic volume index (p=0.035) and lower LV mass index (LVMI) (p=0.037). Pre-TAVI stress global endocardium-epicardium gradient was 0.88±0.09 and global myocardial perfusion reserve (MPR) 2.0±0.48 in 14 patients (6 LGAS and 8 HGAS patients, no difference between groups). Pre-TAVI, baseline coronary data demonstrated lower augmentation pressure (AP, p=0.035) and augmentation index (AIx, p=0.02) in the LGAS group. LGAS patients also exhibited a shorter ejection time (p=0.015), larger forward compression waves during rest, hyperaemia and rapid pacing, and smaller backward expansion waves (BEW) (p=0.001). Lower baseline end systolic pressure (p=0.004), inotropy (dP/dt+, p=0.045), lusitropy (dP/dt-, p=0.069), and stroke work (p=0.019) were observed in the LGAS group. Whilst LV size was smaller the LGAS group, rapid pacing induced a more significant drop in end systolic volume (p=0.045) and ejection fraction (p=0.015) in patients with HGAS. Post-TAVI, the hyperaemic BEW fell sharply (p<0.001), along with coronary VTI (p=0.02), and average pulse velocity (p=0.028), and AP and AIx remained lower (p=0.034 and p=0.031, respectively). The forward expansion wave was reduced in LGAS during rapid pacing. The HGAS group displayed a more profound drop in dP/dt+ (p=0.011) and dP/dt- p=0.014) at rest following intervention. Repeat CMR demonstrated statistically significant reduction in LV size and LVMI (p=0.012 and p<0.001, respectively) with significant increase in 3D global peak radial, circumferential and longitudinal strain (p=0.004, p=0.001 and p=0.018, respectively). Post-TAVI stress global endocardium-epicardium gradient was 0.88±0.13 and MPR 2.46±0.59 (improved from pre-TAVI, p=0.05). There was no difference in remodelling patterns or perfusion between the two groups. Conclusion This is the first study detailing the combined invasive and CMR pathophysiological changes in LGAS. Despite invasive parameters indicating a disease of less severe AS, the level of perfusion abnormality is disproportionate which may in part, relate to their adverse prognosis. Acknowledgement/Funding This research is funded by a Clinical Research Training Fellowship grant from the British Heart Foundation (FS/16/51/32365).

Tachycardia-induced cardiomyopathy: effects on blood flow and capillary structure

1991 ◽  
Vol 261 (1) ◽  
pp. H140-H148 ◽  
Author(s):  
F. G. Spinale ◽  
J. L. Zellner ◽  
M. Tomita ◽  
G. E. Tempel ◽  
F. A. Crawford ◽  
...  
Keyword(s):  
Blood Flow ◽  
Capillary Density ◽  
Left Ventricular ◽  
Lv Function ◽  
Atrial Pacing ◽  
Capillary Structure ◽  
Potential Factor ◽  
Rapid Pacing ◽  
Tachycardia Induced Cardiomyopathy ◽  
Fractional Shortening

Chronic supraventricular tachycardia (SVT) causes a dilated cardiomyopathy. A potential factor contributing to the development of SVT-induced cardiomyopathy is abnormal myocardial blood flow (MBF). The purpose of this study was to relate changes in left ventricular (LV) function, MBF, and capillary structure with the development of SVT-induced cardiomyopathy. LV function and MBF were measured in two groups of conscious pigs: sham control (CON; n = 8) and after 3 wk of atrial pacing (SVT; 240 beats/min; n = 8) using echocardiography-catheterization and microspheres. Measurements were made under three states: 1) at rest with a basal heart rate, 2) during rapid atrial pacing (240 beats/min), and 3) during adenosine infusion (1.5 microM.kg-1.min-1) without pacing. LV capillary density, diameter, wall thickness, and capillary-myocyte distance were measured in four additional pigs from each group. LV fractional shortening was lower, and left atrial pressure was significantly higher in the SVT group compared with CON at rest, during pacing, and with adenosine (P less than 0.05). In the CON group, average LV-MBF at rest was 2.0 +/- 0.2 ml.min-1.g-1, increased with pacing to 3.0 +/- 0.2 ml.min-1.g-1 (P less than 0.05), and increased further with adenosine to 4.1 +/- 0.3 ml.min-1.g-1 (P less than 0.05). In all states, SVT LV-MBF was significantly reduced vs. CON (P less than 0.05); SVT LV-MBF was 0.8 +/- 0.2 ml.min-1.g-1 at rest, increased to 1.3 +/- 0.3 ml.min-1.g-1 with rapid pacing (P less than 0.05), and remained unchanged during adenosine (1.3 +/- 0.4 ml.min-1.g-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac catheterization and intervention

2012 ◽  
Keyword(s):  
Vascular Access ◽  
Right Heart Catheterization ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Site Management ◽  
Access Site ◽  
Angiographic Study ◽  
Right Heart ◽  
Catheterization Laboratory ◽  
Complications Of Angiography

Radiation protection in the catheterization laboratory 310Vascular access: the femoral artery 312Vascular access: the radial artery 314Vascular access site management 316Coronary angiography 318Interpreting the coronary angiogram 320Angiographic study of grafts 322Complications of angiography 324Right-heart catheterization 326Cardiac output and left ventricular function ...

Ryanodine receptor dysfunction and triggered activity in the heart

2007 ◽  
Vol 292 (5) ◽  
pp. H2144-H2151 ◽  
Author(s):  
Rodolphe P. Katra ◽  
Toshiyuki Oya ◽  
Gregory S. Hoeker ◽  
Kenneth R. Laurita
Keyword(s):  
Ryanodine Receptor ◽  
Transmembrane Potential ◽  
Calcium Release ◽  
Left Ventricular ◽  
Calcium Handling ◽  
Adrenergic Stimulation ◽  
Triggered Activity ◽  
Multiple Regions ◽  
Rapid Pacing ◽  
Almost All

Arrhythmogenesis has been increasingly linked to cardiac ryanodine receptor (RyR) dysfunction. However, the mechanistic relationship between abnormal RyR function and arrhythmogenesis in the heart is not clear. We hypothesize that, under abnormal RyR conditions, triggered activity will be caused by spontaneous calcium release (SCR) events that depend on transmural heterogeneities of calcium handling. We performed high-resolution optical mapping of intracellular calcium and transmembrane potential in the canine left ventricular wedge preparation ( n = 28). Rapid pacing was used to initiate triggered activity under normal and abnormal RyR conditions induced by FKBP12.6 dissociation and β-adrenergic stimulation (20–150 μM rapamycin, 0.2 μM isoproterenol). Under abnormal RyR conditions, almost all preparations experienced SCRs and triggered activity, in contrast to control, rapamycin, or isoproterenol conditions alone. Furthermore, under abnormal RyR conditions, complex arrhythmias (monomorphic and polymorphic tachycardia) were commonly observed. After washout of rapamycin and isoproterenol, no triggered activity was observed. Surprisingly, triggered activity and SCRs occurred preferentially near the epicardium but not the endocardium ( P < 0.01). Interestingly, the occurrence of triggered activity and SCR events could not be explained by cytoplasmic calcium levels, but rather by fast calcium reuptake kinetics. These data suggest that, under abnormal RyR conditions, triggered activity is caused by multiple SCR events that depend on the faster calcium reuptake kinetics near the epicardium. Furthermore, multiple regions of SCR may be a mechanism for multifocal arrhythmias associated with RyR dysfunction.

Left atrial systolic and diastolic function accompanying chronic rapid pacing-induced atrial failure

1998 ◽  
Vol 275 (1) ◽  
pp. H183-H189 ◽  
Author(s):  
Brian D. Hoit ◽  
Yanfu Shao ◽  
Marjorie Gabel
Keyword(s):  
Left Atrial ◽  
Time Derivative ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Reduced Ejection Fraction ◽  
Stiffness Constant ◽  
Ventricular Response ◽  
Rapid Pacing ◽  
Systolic And Diastolic Function ◽  
Conduit Function

The objective of this study was to examine the hypothesis that long-term, rapid atrial pacing produces a model of atrial systolic and diastolic dysfunction but does not alter ventricular function. Eight dogs were atrially paced at 400 beats/min (3:1–5:1 ventricular response) for 6 wk and subsequently instrumented with left atrial (LA) and left ventricular (LV) sonomicrometers and micromanometers. Data were compared with those from six sham-operated controls at matched heart rates and mean LA pressures of 10 mmHg. Dogs with rapid pacing had slightly greater LA volume (10.3 ± 4.0 vs. 7.9 ± 4.4 ml) and reduced ejection fraction (2.2 ± 1.4 vs. 13.0 ± 4.0, P < 0.05), systolic ejection rate (0.3 ± 0.1 vs. 2.8 ± 1.2 vol/s, P < 0.05), and reservoir fraction (0.07 ± 0.04 vs. 0.35 ± 0.06, P < 0.05) compared with controls. LA diastolic chamber stiffness was greater after rapid atrial pacing than before (stiffness constant k c, 5.7 ± 2.3 vs. 3.4 ± 0.6, P < 0.05), and the ratio of transesophageal echo-determined pulmonary venous systolic to diastolic integrated flow (a measure of relative reservoir to conduit function of the LA) was less in rapidly paced dogs compared with control dogs (0.41 ± 0.19 vs. 0.68 ± 0.23, P < 0.05). In contrast, rapid atrial pacing did not influence LV systolic performance or lusitropy, because the LV pressure time derivative and the time constant of LV relaxation were similar in both groups. In this model of isolated atrial myopathy, increased atrial stiffness and enhanced conduit function compensate for impaired atrial booster pump and reservoir functions.

scholarly journals Aortic Valve Predilatation with a Small Balloon, without Rapid Pacing, prior to Transfemoral Transcatheter Aortic Valve Replacement

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Anupama Shivaraju ◽  
Christian Thilo ◽  
Neal Sawlani ◽  
Ilka Ott ◽  
Heribert Schunkert ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Replacement ◽  
Valve Replacement ◽  
Transcatheter Aortic Valve Replacement ◽  
Severe Aortic Stenosis ◽  
Chronic Atrial Fibrillation ◽  
Left Ventricular ◽  
Transcatheter Aortic Valve ◽  
Rapid Pacing ◽  
The Mean

Objectives. The aim of this study is to assess the feasibility and clinical outcome of transcatheter aortic valve replacement (TAVR) using aortic valve predilatation (AVPD) with a small, nonocclusive balloon. Background. Balloon aortic valvuloplasty (BAV) under rapid pacing is generally performed in TAVR to ensure the passage and sufficient deployment of the prosthesis in the stenotic AV. BAV may cause serious complications, such as left ventricular stunning or cerebrovascular embolism. Methods. A cohort of 50 consecutive patients with severe aortic stenosis underwent transfemoral TAVR with the Edwards Sapien 3-heart valve. All patients underwent AVPD with a small, nonocclusive balloon (12 × 60 or 14 × 60 mm) without rapid pacing. Procedural data and clinical outcomes were analyzed. Results. The mean age of the cohort was 81±6 years and the mean logistic EuroSCORE (European System for Cardiac Operative Risk Evaluation) was 13±9. Crossing the AV and prosthesis implantation was successful in all cases. The postprocedural mean AV gradient was 12±5 mmHg. There were no cases of aortic regurgitation ≥ grade 2. No periprocedural stroke occurred. One patient (2%) with chronic atrial fibrillation displayed a transient Wernicke aphasia occurring more than 24 hours after TAVR. Mortality was 0% at 30 days after procedure. Conclusion. In TAVR, AVPD with a small, nonocclusive balloon can be safely performed. By avoiding rapid pacing, this technique may be a valid alternative to traditional BAV. Whether or not the use of APVD without rapid pacing translates into less periprocedural complications needs to be assessed in future studies.

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