Left ventricular asynergy during intracoronary isoproterenol infusion in dogs

1980 ◽  
Vol 239 (5) ◽  
pp. H594-H600
Author(s):  
A. Ilebekk ◽  
J. Lekven ◽  
F. Kiil

Myocardial contractions were examined in the left ventricle of anesthetized, open-chest dogs during infusion of a beta-adrenergic agent, isoproterenol (0.1-0.5 micrograms/min) into a shunt line to the left anterior descending coronary artery. Myocardial chord lengths were continuously monitored by pairs of ultrasonic elements inserted into the isoproterenol-infused and control regions. Heart rate remained constant, but isoproterenol altered contraction patterns in both control and infused regions. Contraction in the infused region started before ejection and stretched the control myocardium in early systole. Because of early relaxation, however, the infusion region was stretched at the end of ejection and in early diastole, while the control myocardium continued to shorten. Thus, isoproterenol infusion to a part of the left ventricle induces asynergic muscle contractions and despite localized inotropic stimulation stroke volume may not be significantly increased.

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.


Author(s):  
Mostafa Hamed Mostafa Elbahnasy ◽  
Ibtsam Khairat Ibrahim ◽  
Ehab Abdel Latef El Gendy ◽  
Ehab Abdel Wahab Hamdy

Background: Left ventricular dysfunction is the single strongest predictor of mortality and one of the most frequent and deadly complication following coronary artery diseases. Aim: This   work   aims   to   study   and  explore  the  left  ventricle  ejection  fraction  improvement  after revascularization  with percutaneous coronary intervention (PCI) and the predictive factors for left ventricle ejection fraction improvement. Methods: One hundred patients with ischemic (HFrEF) who had complete revascularization with percutaneous coronary intervention (PCI), had survived at least 90 days and had undergone echocardiography review. The study duration was 1 year from April 2019 to May 2020. Result: We focused on a group of the common possible predictive factors affecting left ventricular improvement. Gender (male), CKD, DM, number of affected vessel(single vessel disease), CTO lesion, heart rate, ECG findings, presence of anginal pain, presence of dyspnea , usage of medications ( ACEI and Clopidogrel),hyper urecemia and the time between presentation of complaints and PCI were correlated with improvement of left ventricular function after revascularization by PCI. Conclusion: Time between appearance of symptoms and PCI was found to be independent predictor of LV EF improvement after revascularization. Other predictors were Male gender, DM, CKD, normal ECG finding ,absence of hyper urecemia, slower heart rate ,presence of chest pain and dyspnea , absence of CTO lesion , single vessel affection and administration of ACEI and Clopidogrel.


2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.


2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Murat Yuksel ◽  
Abdulkadir Yildiz ◽  
Mustafa Oylumlu ◽  
Nihat Polat ◽  
Halit Acet ◽  
...  

Coronary cameral fistulas are abnormal communications between a coronary artery and a heart chamber or a great vessel which are reported in less than 0.1% of patients undergoing diagnostic coronary angiography. All three major coronary arteries are even less frequently involved in fistula formation as it is the case in our patient. A 68-year-old woman was admitted to cardiology clinic with complaints of exertional dyspnea and angina for two years and a new onset palpitation. Standard 12-lead electrocardiogram revealed atrial fibrillation (AF) with a ventricular rate of 114 beat/minute and accompanying T wave abnormalities and minimal ST-depression on lateral derivations. Transthoracic echocardiographic examination was normal except for diastolic dysfunction, minimally mitral regurgitation, and mild to moderate enlargement of the left atrium. Sinus rhythm was achieved by medical cardioversion with amiodarone infusion. Coronary angiography revealed diffuse and multiple coronary-left ventricle fistulas originating from the distal segments of both left and right coronary arterial systems without any stenosis in epicardial coronary arteries. The patient’s symptoms resolved almost completely with medical therapy. High volume shunts via coronary artery to left ventricular microfistulas may lead to increased volume overload and subsequent increase in end-diastolic pressure of the left ventricle and may cause left atrial enlargement.


1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.


Author(s):  
M. O. Chyzh ◽  
A. O. Manchenko ◽  
A. V. Trofimova ◽  
I. V. Belochkina

Background. Late seeking medical advice, limited number of cardiac surgery hospitals and conservative treatment, which does not seem to be always efficacious, trigger the search for new, more effective mode therapy of acute myocardial infarction (MI). Recently, mesenchymal stromal cells (MSCs) have come into sharp focus of scientists due to the prospects for clinical use. On the other hand, multicenter studies have proved that therapeutic hypothermia (TH) has neuro- and cardioprotective effects, and it is administered as one of the urgent methods in providing primary health care. Purpose. Providing and analyzing ultrasonography (US) of rat hearts with experimental MI in order to determine the nature of heart remodelling under combined use of TH and introducing allogeneic MSCs. Materials and methods. The study involved 90 outbred white rats weighing 240–270 g. Myocardial infarction was reproduced by ligating the descending branch of the left coronary artery on the border of the upper and middle third of the vessel. Therapeutic hypothermia was performed in a cold chamber, 60 minutes long. The local skin temperature of the neck area was maintained at +4 оC, while the rectal and tympanic temperature decreased to + 25 оC. A suspension of allogeneic cryopreserved MSCs of the placenta with a concentration of 1.2 × × 106 cells/ml was administered once intravenously through v. saphena magna. Heart sonography was carried out by means of «Сономед 500» («СПЕКТРОМЕД», Russia) ultrasound scanner in B- and M-mode using a linear sensor 7.5L38 with frequency of 7.5 MHz. Results and discussion. The control group with experimental MI showed significantly suppressed function of the left ventricle (LV). It resulted in decreasing stroke volume (SV) and cardiac output (CO) and on the whole indicated reduced ejection fraction (EF) to 46.04 %, that was 35 % less than the corresponding normal range. According to the values of relative wall thickness (RWT) and left ventricular mass (LVM) on day 7 and day 30 after ligating the left coronary artery, LV remodelling was proceeding via eccentric mode of LV alteration. Therapeutic hypothermia was not able to completely stop the pathophysiological processes associated with coronary ligation. EF was not significantly different from the control group, and was 51.08 ± ± 2.68 %. On day 7 of the experiment, heart remodelling in this group was proceeding according to the normal geometry model, and on day 30 – according to the eccentric model. In spite of the volume overload causing post-infarction extension of the left ventricular cavity, in the group with applying MSCs, on day 7 there was a compensatory increase of the stroke volume, 1.8 times over compared to the group with normal range values and 2.3 over compared to the control group. The ejection fraction was 17 % less than the normal range, but statistically significantly higher than the corresponding indicator of the control group of this observation period. Heart remodelling after applying allogeneic MSCs associated with MI at all stages of observation was proceeding by eccentric LV hypertrophy. Аfter therapeutic hypothermia and applying MSCs associated with experimental myocardial infarction on day 7 and day 30, the group recorded the best values of echo params of LV anatomical structures, indicating no dilatation along with occuring moderate myocardial hypertrophy. The ejection fraction showed the best outcome, i. e. 58.78 %, while LV remodelling was minimal, occurring according to normal heart geometry. Conclusions. Applying echocardiography in rats is a very informative diagnosis method which makes it possible to describe the type of structural and functional remodelling of the myocardium associated infarction at early and late observation stages. The ultrasound study showed that the closest to the normal range was the group of animals exposed to therapeutic hypothermia and MSC transplantation. According to LVM and RWT values, in the rats of that group on day 7 and day 30 of the experiment, LV remodelling was characterized by normal geometry.


2019 ◽  
Vol 25 (4) ◽  
pp. 389-406 ◽  
Author(s):  
E. V. Kokhan ◽  
G. K. Kiyakbaev ◽  
Z. D. Kobalava

Numerous studies have demonstrated the negative prognostic value of tachycardia, both in the general population and in specific subgroups, including patients with coronary artery disease (CAD), arterial hypertension (HTN) and heart failure with preserved ejection fraction (HFpEF). In the latest edition of the European guidlines for the treatment of HTN the level of heart rate (HR) exceeding 80 beats per minute is highlighted as a separate independent predictor of adverse outcomes. However, the feasibility of pharmacological reduction of HR in patients with sinus rhythm is unclear. Unlike patients with reduced ejection fraction, in whom the positive effects of HR reduction are well established, the data on the effect of pharmacological HR reduction on the prognosis of patients with HTN, CAD and/or HFpEF are not so unambiguous. Some adverse effects of pharmacological correction of HR in such patients, which may be caused by a change in the aortic pressure waveform with its increase in late systole in the presence of left ventricular diastolic dysfunction, are discussed. The reviewed data underline the complexity of the problem of clinical and prognostic significance of increased HR and its correction in patients with HTN, stable CAD and/or HFpEF.


1999 ◽  
Vol 84 (7) ◽  
pp. 2308-2313 ◽  
Author(s):  
George J. Kahaly ◽  
Stephan Wagner ◽  
Jana Nieswandt ◽  
Susanne Mohr-Kahaly ◽  
Thomas J. Ryan

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty- two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (Δ) stroke volume index. Maximal work load and Δ heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The Δ stroke volume index, Δ ejection fraction, Δ heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, Δ heart rate, and Δ ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.


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