scholarly journals Losartan Preserves Integrity of Cardiac Gap Junctions and PGC-1 α Gene Expression and Prevents Cellular Apoptosis in Remote Area of Left Ventricular Myocardium Following Acute Myocardial Infarction

2007 ◽  
Vol 48 (4) ◽  
pp. 533-546 ◽  
Author(s):  
Cheuk-Kwan Sun ◽  
Li-Teh Chang ◽  
Jiunn-Jye Sheu ◽  
Chi-Young Wang ◽  
Ali A. Youssef ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Gap Junctions ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Remote Area ◽  
Left Ventricular Myocardium ◽  
Cellular Apoptosis

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.

scholarly journals The Peculiarity of Left Ventricular Remodeling in Patients with Hypertension Developing Acute Myocardial Infarction

2021 ◽  
Vol 6 (1) ◽  
pp. 153-159
Author(s):  
I. M. Fushtey ◽  
◽  
E. V. Sid’ ◽  
V. О. Ivashchuk
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
St Segment Elevation

The purpose of the study was to determine the peculiarity of left ventricular remodeling among patients with hypertension developing acute myocardial infarction. Material and methods. The results of the study are based on the data of a comprehensive examination of 477 patients with coronary artery disease: 280 patients with STEMI (ST-segment elevation myocardial infarction), 91 patients with NSTEMI (non ST-segment elevation myocardial infarction) and the control group consisted of 76 patients with exertional angina (II and III functional class for 38 people). The examination of patients was carried out in the period from 2015 to January 2018 on the basis of the Regional Medical Center for Cardiovascular Diseases of the Zaporozhye Regional Council. All patients (n=477) were comparable in age, social status and gender. The proportion of patients with hypertension was comparable between the groups and amounted to 255 (91.1%) patients with STEMI, 86 (94.5%) with NSTEMI, and 71 (93.4%) patients with stable coronary artery disease. Results and discussion. The development of left ventricular hypertrophy is a long-term process in hypertensive patients. At first, there is a change in the geometry of the left ventricle, since during systole the ventricle tends to take a spherical shape. Further, dilatation of cavities, hypertrophy and an increase in the mass of the left ventricular myocardium, replacement of the myocardium with fibrous tissue develop. Whereas in patients with acute myocardial infarction, due to acute myocardial ischemia, thickening of the myocardial wall is associated with interstitial edema occurs rather quickly. These important factors make it difficult to compare different studies and to reliably identify patients with true left ventricular hypertrophy. Therefore, left ventricular myocardium mass index should be determined as early as possible in patients with hypertension after the development of acute myocardial infarction, in order to interpret the obtained data. Сonclusion. Ischemic heart disease is often associated with essential hypertension, more than 90% of patients with acute myocardial infarction developed essential hypertension. It was determined that eccentric and concentric left ventricular hypertrophy prevailed among those examined on the first day of hospitalization and was due to the presence of hypertension

scholarly journals Exertional dyspnea after myocardial infarction: thinking beyond the diagnosis of heart failure

2018 ◽  
Vol 46 (11) ◽  
pp. 4769-4774
Author(s):  
Konstantinos Koutsampasopoulos ◽  
Savvas Grigoriadis ◽  
Ioannis Vogiatzis
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Left Ventricular Myocardium ◽  
Inferior Wall ◽  
Delayed Presentation ◽  
Exertional Dyspnea ◽  
St Elevation

Introduction We herein present an unusual case of a pseudoaneurysm of the left ventricular myocardium, which is a rare and fatal complication of myocardial infarction. Case report A 64-year-old man with a history of bipolar disorder and arterial hypertension was hospitalized for delayed presentation ST-elevation myocardial infarction. He was admitted to our hospital 24 hours after symptom onset. Diagnostic coronary angiography revealed 95% stenosis at the distal third of the right coronary artery, and he underwent a primary percutaneous coronary intervention to the culprit lesion. Despite administration of a diuretic and optimization of other pharmaceutical treatment, his heart failure deteriorated. Electrocardiography showed a sinus rhythm with Q-wave formation in the inferior wall leads (II, III, aVF), T-wave inversion in the same leads, and borderline QT prolongation (QTc of 490 ms). No ST elevation suggestive of left ventricular aneurysm formation was noticed. Forty days later, cardiac ultrasound revealed a dyskinetic cavity (pseudoaneurysm) in continuity with the posterior–inferior wall of the myocardium, resulting in severe mitral valve regurgitation. Unfortunately, the patient died while awaiting surgical treatment. Conclusion Although most patients with left ventricular pseudoaneurysm have a relatively benign outcome, those with symptoms of heart failure must be urgently diagnosed and treated.

scholarly journals Successful Surgical Treatment of Postinfarction Rupture of Left Ventricular Myocardium

2020 ◽  
Vol 9 (1) ◽  
pp. 140-147
Author(s):  
M. K. Mazanov ◽  
N. I. Kharitonova ◽  
A. A. Baranov ◽  
S. Yu. Kambarov ◽  
N. M. Bikbova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Surgical Intervention ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Free Wall ◽  
Fatal Complication ◽  
Widespread Availability ◽  
Complications Of Myocardial Infarction

ABSTRACT. The rupture of the left ventricle free wall is one of the most dangerous complications of myocardial infarction. Due to the widespread availability of echocardiography method, the detection of this fatal complication and the number of lives saved after surgery grew. The survival of patients depends on early diagnosis, stabilization of the patient’s condition, promptness and tactics of surgical intervention. We report a case of successful closure of a rupture of the left ventricle free wall on the 15th day after myocardial infarction.

scholarly journals Cardiac and coronary artery study on sudden death cases in Hospital Canselor Tuanku Muhriz

2021 ◽  
Vol 5 (10) ◽  
Author(s):  
Shih Sheng Soo ◽  
Siti Balkis Budin ◽  
Ismarulyusda Ishak ◽  
Faridah Mohd Nor ◽  
Nur Najmi Mohamad Anuar
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Sudden Death ◽  
Thrombus Formation ◽  
Arterial Occlusion ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Common Presentation ◽  
Acute Mi

Background: Sudden death (SD) is defined as an unexpected natural death within an hour onset of symptoms or unwitnessed death that occurs within 24 hours, which accounts for most cardiovascular deaths in Malaysia. This study aimed to evaluate the extent of histopathological changes in the heart and to study the demographic trend in SD cases in Kuala Lumpur, Malaysia. Methods: Specimens from all SD cases were received from 2017 to 2018 by the Forensic Unit, Hospital Canselor Tuanku Mukhriz (HCTM) were studied. The specimens were the left ventricular myocardium and left anterior descending artery (LAD), which were fixed in 10% formalin with haematoxylin and eosin staining. The tissues were graded histologically based on changes such as arterial occlusion, myocardial infarction, and/or thrombus formation. Results: Out of 545 medicolegal deaths, only 25 cases (4.6%) had samples available for analysis. Among these 25 patients, 24 (96%) were male patients and only one (4%) was a female patient. The available samples were from patients aged between 30 to 79 years old. In terms of ethinicity, Malays (40%) were the most numerous, followed by patients of Chinese and Indian ethnicities.The majority of the SD cases had a body mass index (BMI) that ranged between underweight (56%) and obese (40%). Besides, there were 10 (40%) cases of coronary artery with atheroma and 15 (60%) cases of myocardial infarction. The most common presentation of atherosclerosis was grade III and IV, and acute MI was the most common presentation at death, followed by healed infarcts and old infarcts. Discussion and Conclusion: Our findings reflect worsening risk factor levels in cardiovascular diseases, compounded by demographic trends. Further studies on biomarkers specific for cardiac diseases are warranted to understand imminent sudden cardiac death.

scholarly journals Sex differences in gene expression in response to ischemia in the human left ventricular myocardium

2019 ◽  
Vol 28 (10) ◽  
pp. 1682-1693 ◽  
Author(s):  
Gregory Stone ◽  
Ashley Choi ◽  
Oliva Meritxell ◽  
Joshua Gorham ◽  
Mahyar Heydarpour ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium

Abstract P112: Decreased α-Myosin Expression is Associated with Left Ventricular Hypertrophy in Hypertensive Caribbean Vervets

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Chelsea C Weaver ◽  
Anthony Gutierrez ◽  
Jeffrey L Osborn
Keyword(s):  
Gene Expression ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Cardiac Fibrosis ◽  
Peripheral Resistance ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Protein Isoforms ◽  
Left Ventricular Myocardium ◽  
Human Heart Failure

Caribbean vervets ( Chlorocebus aethiops sabeus ) develop hypertension (HT; Systolic Blood Pressure ≥ 140 mmHg) in over 30% (125/345) of the outbred population. Elevated total peripheral resistance in HT increases cardiac afterload, which may lead to left ventricular hypertrophy (LVH) and cardiac remodeling. We hypothesize that prolonged spontaneous HT is associated with LVH, cardiac and aortic fibrosis, as well as differential transcription of myocardial contractile proteins. Vervets were characterized as HT (SBP = 170 ± 25.3 mmHg; n=125) or normotensive (NT, SBP = 99 ± 14.5 mmHg; n=148) using forearm plethysmography (ketamine sedated;15 mg/kg i.m.). Cardiomyocyte cross-sectional area was greater in HT compared to NT animals (HT 283 ± 52 μm 2 , n=9 vs NT 114 ± 8 μm 2 , n=10; p<0.01). Average collagen stained as a function of tissue area was similar in left ventricular myocardium of HT and NT animals (HT 14.17 ± 3.13% or 0.17/1.21 mm 2 , n=9 vs NT 12.22 ± 0.80% or 0.16/1.27 mm 2 , n=10; p>0.05). Aortic adventia collagen area was greater in HT compared to NT vervets (HT 66.12 ± 4.22% or 0.60/0.90 mm 2 , n=6 vs NT 54.53 ± 2.21% or 0.56/1.02 mm 2 , n=10; p<0.05). Total tissue collagen was estimated using a hydroxyproline assay. Collagen content was not different between HT and NT vervets for left ventricular myocardium (HT 194.02 ± 8.61 μg/mL, n=11 vs NT 201.70 ± 18.89 μg/mL, n=10; p=0.71) or aorta (HT 745.64 ± 44.49 μg/mL, n=11 vs NT 668.39 ± 31.06 μg/mL, n=11; p=0.17). Myosin gene expression (α and β) was estimated using RT-PCR of mRNA in left ventricular myocardium of NT (SBP = 98.91 ±10.89 mmHg; n=20) and HT (SBP = 171.51 ± 30.28 mmHg; n=17) vervets. α-myosin was downregulated in HT compared to NT vervets (HT RQ = 0.10 ± 0.03 vs. NT RQ = 0.22 ± 0.04; p<0.05), while β-myosin expression was not different (HT RQ = 0.22 ± 0.17 vs. NT RQ = 0.20 ± 0.16; p=0.83). Thus, spontaneous HT in outbred vervets induces LVH in response to factors other than cardiac fibrosis. Myosin gene expression may shift from α-myosin to other contractile protein isoforms, characteristic of human heart failure. In this nonhuman primate model, HT does not induce significant aortic fibrosis that may occur in aged animals. Future studies will further characterize contractile and pro-inflammatory proteins in LVH of spontaneous HT vervets.

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