scholarly journals Особенности показателей ЭКГ у лиц моложе 45 лет, перенесших инфаркт миокарда

2017 ◽  
Vol 7 (4) ◽  
pp. 240-247
Author(s):  
O. V. Filatova ◽  
E. Ivanova ◽  
V. Chursina
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Left Atrium ◽  
Left Ventricular ◽  
The Body ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
The Right

We conducted a retrospective study of EchoCG from 33 males who had the myocardial infarction. Patients with a diagnosis of "neurocirculatory dystonia" (30 people) entered the control group. We studied the size of the left ventricle, the left atrium, the right ventricle, their relationship to each other, the mass of the myocardium and the mass index of the myocardium of the left ventricle. The study of the morphological structures of the heart revealed a change in the size of the left ventricle, the left atrium and the right ventricle in patients who had an acute myocardial infarction, manifested by an increase in the end-diastolic and end-systolic dimensions of the left ventricle, the left atrium, and the right ventricle. In 2/3 of the patients who had an acute myocardial infarction, the normal geometry of the left ventricle was observed. Around one-quarter of the patients had a concentric remodeling (24%), an eccentric hypertrophy of the left ventricle was the least common (15%). The heart of patients who had an acute myocardial infarction demonstrates a lower functionality being compared to the subjects in the control group. In these groups, the maximum value of the DAC / DDR ratio is observed, the ejection fraction is reduced. To a greater extent, the onset of acute myocardial infarction was determined by the size and mass of the left ventricular myocardium. Important meaning had also the body weight, BMI, surface area of the body, the size of the left atrium, and the right ventricle.

A prosthetic myocardium for repair of localized defects of the left ventricle: Concept and hemodynamic feasibility

1980 ◽  
Vol 3 (3) ◽  
pp. 173-179
Author(s):  
A. Kantrowitz ◽  
T. Igari ◽  
I. Hayashi ◽  
P.S. Freed
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Experimental Investigation ◽  
Left Ventricle ◽  
Treatment Plan ◽  
Surgical Excision ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Surgical Approaches ◽  
Left Ventricular Myocardium

As an approach to the treatment of patients with large but circumscribed akinetic or dyskinetic regions in the left ventricular myocardium as sequelae of acute myocardial infarction, excision of the defect and implantation of a mechanical functional equivalent of myocardium is suggested. Experimental investigation of this technique is described. Hemodynamic data from a series of dog experiments indicate that activation of the prosthetic myocardium after excision of the left ventricle is followed by improvement in various hemodynamic parametres of interest Although substantial experimental work must be completed and difficult bioengineering problems solved, preliminary results have encouraged us to continue our investigations of the prosthetic myocardium. An imposing array of treatment methods is now available to the clinician who must deal with the sequelae of acute myocardial infarction. Selecting from pharmacologic, electrophysiologic, and surgical approaches the physician can in many instances design a treatment plan precisely tailored to the clinical problem. Large left ventricular aneurysms and their functional equivalents of ventricular dyskinesis or hypokinesis continue, however, to represent a class of problems in which established techniques have been less then satisfactory. Surgical excision with closure of the defect is regarded as effective for small aneurysms, but such procedures may so compromise cardiac output in patients with large ones as to be unacceptable. Unfortunately, it is just the latter group in which medical palliation is least likely to be effective in managing congestive failure, angina, and other pathophysiologic manifestations. A relatively unsual approach derived from in-series techniques of mechanical assistance to the failing circulation (1) offers the theoretical possibility of a treatment tailored to the problem of a large ventricular aneurysm. Experimental investigation of this technique in the Surgical Research Laboratory at the Sinai Hospital of Detroit has progressed to the point that a report of our experiences to date may be of interest.

Difficulties in diagnosing the myocardial infarction of the left ventricle inferior wall involving the right ventricle

2021 ◽  
Vol 19 (1) ◽  
pp. 82-85
Author(s):  
S. D. Mayanskaya ◽  
◽  
A. A. Gilmanov ◽  
T. V. Rudneva ◽  
M. M. Mangusheva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Left Ventricular ◽  
Inferior Wall ◽  
Jugular Veins ◽  
St Segment Elevation ◽  
St Segment ◽  
The Right ◽  
Negative Predictor

The article presents a clinical observation of myocardial infarction (MI) of the inferior wall of the left ventricle (LV) with ST-segment elevation in combination with damage to the right ventricle (RV). Unfortunately, there is often a delay in the timely diagnosis of RV involvement in the process. This is because, at the beginning of the symptoms, it may not differ clinically from the typical manifestations of MI of the inferior-diaphragmatic region of the LV. However, the combination of LV inferior wall MI with RV MI is an important, negative predictor of increased mortality in these patients. In this case, RV MI was diagnosed after stenting of the right coronary artery, only when signs of hypotension and increased pressure of the jugular veins appeared. Based on the analysis of this clinical case, the authors discuss the need to record an ECG of the right heart in most patients with inferior MI, especially in the presence of hypotension without signs of acute left ventricular failure.

Left ventricular failure induced by myocardial infarction. II. Tissue morphometry

1985 ◽  
Vol 248 (6) ◽  
pp. H883-H889 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Volume Fraction ◽  
Volume Ratio ◽  
Left Ventricular ◽  
Tissue Growth ◽  
Left And Right ◽  
The Right ◽  
And Diffusion

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.

scholarly journals P262 Left ventricular pseudoaneurism due to a non-reperfused myocardial infarction: multi-modality cardiac imaging approach

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
J A Fuentes Mendoza ◽  
O A Mondaca Garcia ◽  
N G Espinola Zavaleta
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Left Ventricle ◽  
Left Ventricular ◽  
Medical Attention ◽  
Inferior Wall ◽  
Risk Of Rupture ◽  
The Right

Abstract Introduction Cardiac rupture has been one of the most frequent fatal complications of acute myocardial infarction in cases series reported since 1977. However, in exceptional cases, the rupture of the left ventricle is contained by the pericardium and by fibrous tissue, forming a pseudoaneurysm, which is characterized by the absence of myocardial tissue in its wall and a relatively narrow neck between the ventricle and the ventricular chamber. Although there is no estimated time for rupture, it is well established that the risk of rupture is 30 to 40% and mortality up to 10%. Pseudoaneurysm is a rarer entity than rupture and is usually diagnosed incidentally by imaging methods in up to 48% of cases. The most frequent imaging method for their diagnosis is 2D echocardiography, followed by cardiac catheterization and finally cardiac magnetic resonance. The most frequent location of the pseudoaneurysm secondary to acute myocardial infarction is the inferior wall and the posterolateral wall of the left ventricle. Case Report We present 72-year-old male patient with a history of type 2 diabetes and smoking, who started symptoms with sudden onset of oppressive chest pain of 20 minutes duration, he did not attend medical attention. A month later, he went for a valuation with a first-contact physician, who referred him to our institution with a diagnosis of acute myocardial infarction without reperfusion therapy. At the initial assessment, it was found asymptomatic, in the resting ECG was found QS pattern with reversal of the T wave in leads DII, DIII and AVF. Cardiac SPECT was performed and showed an inferior transmural infarction, which extended as non-transmural to the inferolateral and inferoseptal walls, without ischemia. (Img. 1 and 2). A 2D and 3D transthoracic echocardiogram was performed, in which akinesia of the inferoseptal and apical walls was documented, as well as a saccular pseudoaneurysm of 5.6 X 4.7 cm in the basal and middle segment of the inferior and inferolateral walls, with an entrance orifice. 2.6 X 2.4 cm, as well as pericardial effusion. (Fig. 3 and 4). Coronary angiography was performed, demonstrating chronic total occlusion of the right coronary in its proximal segment and ostial obstruction of the left anterior descending. Cardiac magnetic resonance revealed inferior infarction and the presence of a pseudoaneurysm with lamellar thrombus was corroborated. (Img. 5). The patient was taken to surgical treatment, by reconstruction of the left ventricle with the Dor technique and CABG of the right coronary artery and the anterior descending artery. Receives medical treatment and a 1-month follow-up is in class I of the NYHA. Conclusion It is a clinical case about a potentially fatal complication of acute myocardial infarction, which in our case was detected incidentally since the patient had remained asymptomatic, there lies the importance of obtaining an accurate diagnosis in order to impact on the patient survival. Abstract P262 Figure. Pseudoaneurysm multi-modality images

Localization of preproenkephalin mRNA in rat heart: selective gene expression in left ventricular myocardium

1998 ◽  
Vol 275 (2) ◽  
pp. H378-H384 ◽  
Author(s):  
Joachim Weil ◽  
Thomas Eschenhagen ◽  
Gerrit Fleige ◽  
Clemens Mittmann ◽  
Ellen Orthey ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Opiate Receptors ◽  
Ventricular Myocardium ◽  
Northern Blotting ◽  
Postnatal Period ◽  
Left Ventricular ◽  
The Body ◽  
Left Ventricular Myocardium ◽  
Mrna Levels ◽  
The Right

The enkephalins are derived from a common precursor protein known as preproenkephalin (ppENK). Enkephalins appear to be one of the endogenous ligands for the opiate receptors. In the rat the ventricular myocardium contains more ppENK mRNA than any other tissue. To gain further insight into the role of cardiac enkephalins, the regional and developmental distribution of ppENK mRNA was studied by Northern blotting and in situ hybridization. In the early postnatal period, ppENK mRNA is low in atrial and ventricular myocardium. With maturation, ppENK expression increases threefold in left and right ventricular tissue, but not in the atria or cardiac conductive system. Interestingly, ppENK mRNA levels are four times higher in the left than in the right chamber. Thus, to our knowledge, ppENK is the only gene exhibiting marked differences in expression between the adult right and left ventricle. Given the left-side preference of ppENK expression, the possibility is raised that the left ventricle is an endocrine organ that supplies the body with enkephalins.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

scholarly journals Plasma Level of High-Sensitive C-Reactive Protein in Patients with Acute Myocardial Infarction and Arterial Hypertension

2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Wael Rumaneh
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Level ◽  
Arterial Hypertension ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Control Group ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein

Arterial hypertension is an independent predictor of acute myocardial infarction. Nowadays, plasma level of high-sensitive C-reactive protein is a marker of cardiovascular risk. The objective of the research was to evaluate plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction and arterial hypertension depending on myocardial remodeling type. Materials and methods. 130 patients with myocardial infarction (63 individuals with concomitant arterial hypertension and 67 individuals without it) were observed. Transthoracic echocardiogram was used. To evaluate plasma level of high-sensitive C-reactive protein the ELISA method was applied. Results. Plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction increased by 5.11 times compared to the control group: (10.67 [5.43; 12.89]) mg/l and (2.09 [1.40; 4.60]) mg/l, respectively (p<0.001). In myocardial infarction and arterial hypertension, this parameter increased by 6.57 times (to (13.73 [7.05; 15.17]) mg/l) (p<0.001), and by 1.27 times (p<0.05) as compared to patients without arterial hypertension. No differences in plasma level of high-sensitive C-reactive protein were detected in patients with different types of left ventricular remodeling.Conclusions. Acute myocardial infarction caused by high plasma level of high-sensitive C-reactive protein is severer in co-existent arterial hypertension. There are no differences in blood levels of high-sensitive C-reactive protein depending on the type of left ventricular remodeling.

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