Effects of insulin on ventricular function in diabetic lambs with acidosis

1981 ◽  
Vol 241 (3) ◽  
pp. H401-H407
Author(s):  
S. E. Downing ◽  
J. C. Lee ◽  
J. C. Werner
Keyword(s):  
No Reduction ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Time Interval ◽  
Inotropic Action ◽  
Mean Values ◽  
Chronic Group ◽  
Acute Group ◽  
Group Data ◽  
Arterial Ph

Diabetes mellitus (DM) was induced in 10 lambs by giving alloxan (150 mg/kg). Two to 4 days later, mean values for glucose were 748 mg/dl, and for arterial pH 7.25 (acute group). Two additional lambs were studied after 3 mo of DM (chronic group). Data were compared with 7 controls (glucose 128 mg/dl, pH 7.36). Left ventricular (LV) performance was assessed from function curves and measurements of LV dP/dtmax. Stroke volume ejected at LV end-diastolic pressure of 5 cmH2O (SV5) was calculated from regression analysis of each curve. SV5 averaged 2.83 +/- 0.34 ml in controls and 2.90 +/- 0.23 ml in the acute diabetics (not significant). Mean values for LV dP/dtmax also did not differ. A significant correlation was found between SV5 and LV weight (P less than 0.001). SV5 was normalized as ml/100 g LV, and average values for the three groups were identical. Insulin (10 U/kg) caused a progressive fall in SV5 in diabetics with severe acidosis (pH 7.00), but not in those with less acidosis (pH 7.28). In nondiabetics given lactic acid (pH 7.01), SV5 fell to 60% of initial values 1 h after insulin. Acidemic animals not given insulin showed no reduction in LV performance in the same time interval. Adrenergic support is necessary to prevent cardiac failure associated with acidosis. The present findings are ascribed to inhibition by insulin of catecholamine inotropic action on myocardium.

scholarly journals Cardiac Triangle Mapping: A New Systems Approach for Noninvasive Evaluation of Left Ventricular End Diastolic Pressure

Fluids ◽  
2019 ◽  
Vol 4 (1) ◽  
pp. 16
Author(s):  
Niema M Pahlevan ◽  
Ray V Matthews
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Systems Approach ◽  
Diastolic Pressure ◽  
Unmet Need ◽  
Left Ventricular ◽  
Time Interval ◽  
Chronic Congestive Heart Failure ◽  
Intrinsic Frequency ◽  
Future Design

Noninvasive and practical assessment of hemodynamics is a critical unmet need in the treatment of both chronic and acute cardiovascular diseases. Particularly, the ability to monitor left ventricular end-diastolic pressure (LVEDP) noninvasively offers enormous benefit for managing patients with chronic congestive heart failure. Recently, we provided proof of concept that a new cardiac metric, intrinsic frequency (IF), derived from mathematical analysis of non-invasively captured arterial waveforms, can be used to accurately compute cardiovascular hemodynamic measures, such as left ventricle ejection fraction (LVEF), by using a smartphone. In this manuscript, we propose a new systems-based method called cardiac triangle mapping (CTM) for hemodynamics evaluation of the left ventricle. This method is based on intrinsic frequency (IF) and systolic time interval (STI) methods that allows computation of LVEDP from noninvasive measurements. Since the CTM method only requires arterial waveform and electrocardiogram (ECG), it can eventually be adopted as a simple smartphone-based device, an inexpensive hand-held device, or perhaps (with future design modifications) a wearable sensor. Such devices, combined with this method, would allow for remote monitoring of heart failure patients.

The role of hypoxemia, vasoactive compounds, and acidemia in the pathogenesis of pulmonary edema in the dog with experimental left ventricular overload

1980 ◽  
Vol 58 (7) ◽  
pp. 849-855
Author(s):  
John S. Baumber
Keyword(s):  
Pulmonary Edema ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Left Heart Failure ◽  
Ventricular Systolic Pressure ◽  
Vasoactive Substances ◽  
Arterial Ph

The pathogenesis of pulmonary edema (PE) in left heart failure involves a consideration of the hydrostatic, osmotic, and permeability changes in the pulmonary circulation. In 14 dogs with isolated left ventricular overload induced by suturing a Teflon graft between the aorta and left atrium, left ventricular end-diastolic pressure (LVEDP) was 36 mmHg (1 mmHg = 133.322 Pa) 3 weeks following surgery. There was no clinical evidence of PE. Seven of these animals developed PE when allowed to breathe 10% O2 in N2 for 15 min. There was no further increase in LVEDP or right ventricular systolic pressure (RVSP). It was postulated that a change in permeability superimposed on increased capillary hydrostatic pressure could result in the overwhelming accumulation of fluid in the alveoli. The release of vasoactive substances from pulmonary mast cells or from the adrenal medulla might alter capillary permeability. However, the infusion of histamine or epinephrine in seven dogs with elevated LVEDP and RVSP failed to precipitate fulminating PE. We have previously observed an increase in plasma renin activity in dogs associated with PE. Nonpressor infusions of angiotensin failed to produce PE. The infusion of lactic acid to decrease the arterial pH to 7.00 (the level observed as a result of hypoxia-induced PE) resulted in fulminating PE. It is concluded that acidemia can be an important factor in the development of severe intra-alveolar pulmonary edema.

Myocardial responses to alpha-adrenoceptor stimulation with methoxamine hydrochloride in lambs

1982 ◽  
Vol 242 (3) ◽  
pp. H405-H410 ◽  
Author(s):  
J. C. Lee ◽  
R. R. Fripp ◽  
S. E. Downing
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Atropine Sulfate ◽  
Left Ventricular ◽  
Inotropic Action ◽  
Ventricular Performance ◽  
Positive Inotropic Action ◽  
Alpha Adrenergic Receptors

This study was undertaken to evaluate the effects of methoxamine on left ventricular performance, coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) in lambs. Measurement of maximum rate of rise of left ventricular pressure (LV dP/dtmax), left ventricular end-diastolic pressure (LVEDP), CBF, and MVO2 were made in nine lambs using a hemodynamically controlled preparation. The lambs were given atropine sulfate (1 mg), tetraethylammonium chloride (100 mg), and practolol (4 mg/kg) to provide parasympathetic, ganglionic, and beta-adrenergic blockades. Aortic pressure and blood flow and heart rate were held constant in each lamb. Dose-related increases in LV dP/dtmax and decreases in LVEDP were observed after progressively larger doses of methoxamine ranging from 0.4 to 6.0 mg/kg were given. These positive inotropic responses were eliminated by giving phentolamine (2 mg/kg). CBF, myocardial O2 extraction, and MVO2 did not change significantly. A positive inotropic action of methoxamine was also demonstrated in five additional animals by obtaining ventricular function curves. Initially the mean stroke volume at LVEDP 10 cmH2O (SV10) was 4.11 +/- 0.16 (SE) ml. This value increased to 5.09 +/- 0.28 ml after methoxamine (P less than 0.01). After phentolamine, SV 10 fell to 4.37 +/- 0.08 ml (P less than 0.05). These observations support the hypothesis that alpha-adrenergic receptors are present and mediate a substantial positive inotropic action on neonatal lamb myocardium.

Cardiovascular responses to metabolic acidosis

1965 ◽  
Vol 208 (2) ◽  
pp. 237-242 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Heart Rate ◽  
Metabolic Acidosis ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Precise Control ◽  
Arterial Ph

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po2, and Pco2 were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.

Non-invasive evaluation of left ventricular filling pressures in patients with abnormal relaxation

2004 ◽  
Vol 106 (5) ◽  
pp. 485-494 ◽  
Author(s):  
Tudor C. POERNER ◽  
Björn GOEBEL ◽  
Petra UNGLAUB ◽  
Tim SÜSELBECK ◽  
Jens J. KADEN ◽  
...  
Keyword(s):  
Relaxation Time ◽  
Predictive Accuracy ◽  
Diastolic Pressure ◽  
Characteristic Curve ◽  
Pulmonary Veins ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Heart Catheterization ◽  
Time Interval ◽  
Non Invasive

The aim of the present study was to assess the ability of several echocardiographic and TDI (tissue Doppler imaging) parameters to predict an elevated LVEDP (left ventricular end-diastolic pressure) in patients with abnormal relaxation. Eighty-two consecutive patients presenting with an E/A ratio (ratio of early-to-late diastolic peak transmitral velocity) <0.9 scheduled for left heart catheterization underwent echocardiography, including TDI, and measurement of LVEDP using fluid-filled catheters. The difference in duration between PVR (retrograde peak in the pulmonary veins) and A (ΔPVR-A) was calculated from pulsed Doppler recordings. VP (propagation velocity of the early mitral inflow) was determined by colour M-mode. TDI measurements included E´ (early diastolic peak myocardial velocities near the lateral mitral annulus), MVG (the early diastolic transmyocardial velocity gradient of the posterior basal wall) and the PRT (peak relaxation time), determined as the time interval between aortic valve closure and peak E´. Fifty-six patients presented with LVEDP values <15 mmHg, whereas an LVEDP >15 mmHg was found in 26 patients. The index ΔPVR-A showed a significant linear correlation with LVEDP (r=0.7, P<0.001) and provided the highest predictive accuracy for the identification of LVEDP >15 mmHg [AUC (area under receiver operating characteristic curve)=0.83], followed by PRT (AUC=0.67), whereas other TDI-derived parameters failed to reach significance. In conclusion, ΔPVR-A enabled the most accurate non-invasive estimation of LVEDP. A prolonged peak relaxation time was the only TDI-derived index that differed significantly between patient groups.

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.

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.

Time interval from left ventricular stimulation to QRS onset is a predictor of mortality in patients with cardiac resynchronization therapy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Yagishita ◽  
Y Yagishita ◽  
S Kataoka ◽  
K Yazaki ◽  
M Kanai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Independent Predictor ◽  
Total Mortality ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Time Interval ◽  
Heart Failure Hospitalization ◽  
Conduction Disturbance ◽  
Secondary Endpoints ◽  
Fibrotic Lesion

Abstract Introduction In our previous report, the time interval from left ventricular (LV) pacing to the earliest onset of QRS (S-QRS interval) has been found to be an independent predictor of mechanical response to cardiac resynchronization therapy (CRT). The S-QRS interval may indicate the conduction disturbance relevant to the localized tissue property such as scar or fibrotic lesion. Therefore, S-QRS interval longer than 37ms was associated with poor response to CRT, and proposed as suboptimal LV lead position. Then, we hypothesized that the longer S-QRS interval at the LV pacing site could be related to long term mortality and heart failure events in patients with CRT. Methods This retrospective study included 82 consecutive heart failure patients with sinus rhythm, reduced LV ejection fraction (≤35%), and a wide QRS complex (≥120ms), who undergone CRT implantation between 2012 January and 2017 December. Patients were divided into Short S-QRS group (&lt;37ms, SS-QRS) and Long S-QRS group (≥37ms, LS-QRS) according to the previously reported optimal cut off value. A responder was defined as one with ≥15% reduction in LV end-systolic volume assessed by echocardiography at 6 months after CRT. The primary endpoint was total mortality, which included LV assist device implantation or heart transplantation. The secondary endpoints included the composite endpoint of total mortality or heart failure hospitalization. Results The study patients were divided into SS-QRS (N=43, age 65.9±13.2 years, 77% male) and LS-QRS (N=39, age 63.0±13.4, 85% male). In the electrocardiographic measurements, there were no significant differences in baseline QRS duration (162.4±30.3ms in SS-QRS vs. 154.5±31.6ms in LS-QRS, P=0.19) and LV local activation time assessed as Q-LV interval (118.3±34.3ms in SS-QRS vs. 115.3±32.0ms in LS-QRS, P=0.71). S-QRS interval was 25.9±5.3ms in SS-QRS and 51.5±13.7ms in LS-QRS (P&lt;0.01), and the responder rate was significantly higher in SS-QRS compared with LS-QRS (79% vs. 29%, P&lt;0.01). During mean follow up of 47.7±22.4 months, 24 patients (29%) reached to the primary endpoint, while the secondary endpoints were observed in 47 patients (57%). LS-QRS patients had significantly worse event-free survival for both primary and secondary endpoints (Figure). After the multivariate Cox regression analysis, LS-QRS (≥37ms) was an independent predictor of total mortality (HR=2.6, 95% CI: 1.11 to 6.12, P=0.03) and the secondary composite events (HR=2.4, 95% CI: 1.31 to 4.33, P&lt;0.01). Conclusion The S-QRS interval longer than 37ms, which may reflect the conduction disturbance relevant to the scar or fibrotic lesion at the LV pacing site, was a significant predictor of the total mortality and heart failure hospitalization. These findings have implications for the optimal LV lead placement in patients with CRT device. Clinical outcomes according to S-QRS Funding Acknowledgement Type of funding source: None

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