Weibull distribution function for cardiac contraction: integrative analysis

1999 ◽  
Vol 277 (5) ◽  
pp. H1940-H1945 ◽  
Author(s):  
Junichi Araki ◽  
Hiromi Matsubara ◽  
Juichiro Shimizu ◽  
Takeshi Mikane ◽  
Satoshi Mohri ◽  
...  
Keyword(s):  
Weibull Distribution ◽  
Systems Engineering ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Weibull Function ◽  
Difference Curve ◽  
First Derivative ◽  
The Difference ◽  
Gradual Pressure

The Weibull distribution is widely used to analyze the cumulative loss of performance, i.e., breakdown, of a complex system in systems engineering. We found for the first time that the difference curve of two Weibull distribution functions almost identically fitted the isovolumically contracting left ventricular (LV) pressure-time curve [P( t)] in all 345 beats (3 beats at each of 5 volumes in 23 canine hearts; r = 0.999953 ± 0.000027; mean ± SD). The first derivative of the difference curve also closely fitted the first derivative of the P( t) curve. These results suggest the possibility that the LV isovolumic P( t) curve may be characterized by two counteracting cumulative breakdown systems. Of these, the first breakdown system causes a gradual pressure rise and the second breakdown system causes a gradual pressure fall. This Weibull-function model of the heart seems to give a new systems engineering or integrative physiological view of the logic underlying LV isovolumic pressure generation.

Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice

2001 ◽  
Vol 281 (5) ◽  
pp. H1938-H1945 ◽  
Author(s):  
Chari Y. T. Hart ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Ketamine Anesthesia ◽  
The Difference ◽  
And Function ◽  
Derivatives Of

Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (τ), and the first derivatives of LV pressure rise and fall (dP/d t max and dP/d t min, respectively). During echocardiography, HR was lower in XK than AV mice (250 ± 14 beats/min in XK vs. 453 ± 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 ± 0.08 mm in XK vs. 3.8 ± 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 ± 1.2% in XK vs. 40 ± 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 ± 24 beats/min) and XK (342 ± 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR <300 beats/min, LVEDP was increased (28 ± 5 vs. 6.2 ± 2 mmHg in mice with HR >300 beats/min, P < 0.05), whereas systolic (LV dP/d t max: 4,402 ± 798 vs. 8,250 ± 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (τ: 23 ± 2 vs. 14 ± 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.

HEART COMPLICATIONS IN HYPERTHYROIDISM

2011 ◽  
pp. 7-17
Author(s):  
Hai Thuy Nguyen ◽  
Anh Vu Nguyen
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Diseases ◽  
Systolic Dysfunction ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Cardiac Complications ◽  
Cardiac Symptoms

Thyroid hormone increases the force of the contraction and the amount of the heart muscle oxygen demand. It also increases the heart rate. Due to these reasons, the work of the heart is greatly increased in hyperthyroidism. Hyperthyroidism increases the amount of nitric oxide in the intima, lead them to be dilated and become less stiff. Cardiac symptoms can be seen in anybody with hyperthyroidism, but can be particularly dangerous in whom have underlying heart diseases. Common symptoms include: tachycardia and palpitations. Occult hyperthyroidism is a common cause of an increased heart rate at rest and with mild exertion. Hyperthyroidism can also produce a host of other arrhythmias such as PVCs, ventricular tachycardia and especially atrial fibrillation. Left ventricular diastolic dysfunction and systolic dysfunction, Mitral regurgitation and mitral valve prolapsed are heart complications of hyperthyroism could be detected by echocardiography. The forceful cardiac contraction increases the systolic blood pressure despite the increased relaxation in the blood vessels reduces the diastolic blood pressure. Atrial fibrillation, atrial enlargement and congestive heart failure are important cardiac complications of hyperthyroidism. An increased risks of stroke is common in patients with atrial fibrillation. Graves disease is linked to autoimmune complications, such as cardiac valve involvement, pulmonary arterial hypertension and specific cardiomyopathy. Worsening angina: Patients with coronary artery disease often experience a marked worsening in symptoms with hyperthyroidism. These can include an increase in chest pain (angina) or even a heart attack.

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.

Doppler-derived left ventricular rate of pressure rise and inotropic requirements during mitral valve surgery

1998 ◽  
Vol 12 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Serge M. Broka ◽  
Anne R. Ducart ◽  
Jacques Jamart ◽  
Edith L. Collard ◽  
Xavier R. Fournet ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Pressure Rise ◽  
Mitral Valve Surgery ◽  
Left Ventricular ◽  
Valve Surgery ◽  
Ventricular Rate

Cardiac contractile injury after intestinal ischemia-reperfusion

1991 ◽  
Vol 261 (4) ◽  
pp. H1164-H1170 ◽  
Author(s):  
J. W. Horton ◽  
D. J. White
Keyword(s):  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Multiorgan Failure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
In Vivo Studies ◽  
Lv Function ◽  
Acid Base Balance ◽  
Cardiac Contractile ◽  
Sequence Of Events

Experimental and clinical data suggest that even a brief period of intestinal ischemia followed by reperfusion initiates a sequence of events that include release of inflammatory mediators and multiorgan failure. In this study, 41 rats were subjected to occlusion of the superior mesenteric artery (SMA) for 20 min and collateral arcade ligation. Twelve rats were sham operated and served as controls (group 1). Groups of rats with SMA occlusion were killed at several time intervals after reperfusion (group 2, 2-3 h; group 3, 4-5 h; group 4, 12-16 h). In group 5, rats were pretreated with enterally administered allopurinol (10 mg.kg-1.day-1) for 4 days before the intestinal ischemia episode and were studied 2-3 h after reperfusion. In vivo studies confirmed that 20 min of intestinal ischemia produced a transient bradycardia (P less than 0.05) and no change in systemic blood pressure, acid-base balance, or hematocrit. In vitro studies showed marked cardiac contractile depression as early as 2 h after ischemia-reperfusion as indicated by a fall in left ventricular pressure (LVP; from 77 +/- 3 to 63 +/- 4 mmHg, P = 0.01) and +dP/dtmax (from 1,827 +/- 59 to 1,557 +/- 99 mmHg/s, P less than 0.02) and -dP/dtmax (from 1,267 +/- 57 to 953 +/- 67 mmHg/s, P = 0.02), a rightward shift in LV function curves, and a decreased responsiveness to perfusate Ca2+. Allopurinol pretreatment prevented ischemia-reperfusion-mediated deficits in cardiac contraction and relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart function after injection of small air bubbles in coronary artery of pigs

1993 ◽  
Vol 75 (3) ◽  
pp. 1201-1207 ◽  
Author(s):  
J. H. Van Blankenstein ◽  
C. J. Slager ◽  
J. C. Schuurbiers ◽  
S. Strikwerda ◽  
P. D. Verdouw
Keyword(s):  
Coronary Artery ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Relative Increase ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Relative Reduction ◽  
Air Bubbles ◽  
First Derivative ◽  
A Minor

By its nature, vaporization of atherosclerotic plaques by laser irradiation or spark erosion may produce a substantial amount of gas. To evaluate the effect of gas embolism possibly caused by vaporization techniques, air bubbles with diameters of 75, 150, or 300 microns, each in a volume of 2 microliters/kg, were selectively injected subproximal in the left anterior descending coronary artery of seven anesthetized pigs (28 +/- 3 kg). Systemic hemodynamics such as heart rate, left ventricular pressure and its peak positive first derivative, and mean arterial pressure did not change after air injection, whereas there was a minor change in peak negative first derivative of left ventricular pressure. After injection of air bubbles there was a maximal relative reduction of systolic segment shortening (SS) in the myocardium supplied by the left anterior descending coronary artery of 27, 45, and 58% for 75-, 150-, and 300-microns bubbles, respectively, and a relative increase of postsystolic SS (PSS) of 148, 200, and 257% for 75-, 150-, and 300-microns bubbles, respectively. Recovery of SS and PSS started after 2 min and was completed after 10 min. A difference in SS and PSS changes between different bubble size injections could be demonstrated. From this study it is clear that depression of regional myocardial function after injection of air bubbles could pass unnoticed on the basis of global hemodynamic measurements.

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa
Keyword(s):  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Structural Characteristics ◽  
Myocardial Dysfunction ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Cross Sectional

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

scholarly journals Time delay to peak left ventricular pressure rise identifies the substrate for dyssynchronous heart failure and detects disease modification with resynchronization- an observational clinical study

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
H Odland ◽  
T Holm ◽  
S Ross ◽  
LO Gammelsrud ◽  
R Cornelussen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Nyha Class ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Cardiac Resynchronization ◽  
Disease Modification ◽  
Volumetric Response

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Norwegian South East Health Authorities Introduction Identification of disease modification prior to implantation of Cardiac Resynchronization Therapy may help select the right patients, increase responder-rates and promote the utilization of CRT. We tested the hypothesis that shortening of time-to-peak left ventricular pressure rise (Td) with CRT is useful to predict long-term volumetric response (End-systolic volume (ESV) decrease &gt;15%) to CRT. Methods Forty-five heart failure patients admitted for CRT implantation with a class I/IIa indication according to current ESC/AHA guidelines were included in the study. Td was measured from onset QRS at baseline and from onset of pacing with CRT. Results Baseline characteristics were mean age 63 ± 10 years , 71% males, NYHA class 2.5, 87% LBBB, QRS duration 173 ± 15ms, EF biplane 31 ± 1%, ESV 144 ± 12mL and end-diastolic volume 2044 ± 14mL. At 6-months follow-up six patients increased ESV by 5 ± 8%, while 37 responders (85%) had a mean ESV decrease of 40 ± 2%.  Responders presented with a higher Td at baseline compared to non-responders (163 ± 4ms vs 119 ± 9ms, p &lt; 0.01). Td decreased to 156 ± 4ms (p = 0.02) with CRT in responders, while in non-responders Td increased to 147 ± 10ms (p &lt; 0.01) with CRT. A decrease in Td of less than +3.5ms from baseline accurately identified responders to therapy (AUC 0.98, p &lt; 0.01, sensitivity 97%, specificity 100%). AUC was 0.92 for baseline Td and a cut-off at 120ms yielded a sensitivity of 100% and specificity of 80% to identify volumetric responders. A linear relationship between the change in Td from baseline and ESV decrease on long term was found (β=-61, R = 0.58, P &lt; 0.01). Conclusions Td at baseline and the shortening of Td with CRT accurately identifies responders to CRT, with incremental value on top of current guidelines, in a population with already high response rates. Td carries the potential to become the marker for prediction of long-term volumetric response in CRT candidates. Abstract Figure.

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