Abid Hussain Laghari
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Abid Hussain Laghari has a total of 17 co-authors. Here are the top co-authors by number of shared publications:
- Abeer AbdulMoati Al-Masri
Department of Physiology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia
1 shared publication - Alessio Rungatscher
Division of Cardiac Surgery, University of Verona Medical Center, 37126 Verona, Italy
1 shared publication - Awais Farhad
Aga Khan Univ, Dept Med, Karachi, Pakistan
1 shared publication - Babar Nagher
Section of Cardiology, Department of Medicine, The Aga Khan University Hospital, Karachi, Pakistan
1 shared publication - Bashar AlBkhoor
Queen Ali Heart Institute, Amman 111881, Jordan
1 shared publication - Daniele Linardi
Department of Surgery, Cardiac Surgery Division, University of Verona Medical School, 37129 Verona, Italy
1 shared publication
Latest Publications
- Open Access
- 1 January 2022
- Published by Asian Society of Cardiovascular Imaging in Cardiovascular Imaging Asia
- Vol. 6 (1) , 22-24
Breast Mass Detected During Cardiac Stress Testing Which Led to Correct Diagnosis and Treatment
- 1 January 2022
- Published by Asian Society of Cardiovascular Imaging in Cardiovascular Imaging Asia
- Vol. 6 (1) , 22-24
Open AccessBreast Mass Detected During Cardiac Stress Testing Which Led to Correct Diagnosis and Treatment
- Open Access
- 11 December 2019
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 20 (24) , 6237
Fingolimod Plays Role in Attenuation of Myocardial Injury Related to Experimental Model of Cardiac Arrest and Extracorporeal Life Support Resuscitation
Background: Sudden cardiac arrest is a major global health concern, and survival of patients with ischemia–reperfusion injury is a leading cause of myocardial dysfunction. The mechanism of this phenomenon is not well understood because of the complex pathophysiological nature of the disease. Aim of the study was to investigate the cardioprotective role of fingolimod in an in vivo model of cardiac arrest and resuscitation. Methods: In this study, an in vivo rat model of cardiac arrest using extracorporeal membrane oxygenation resuscitation monitored by invasive hemodynamic measurement was developed. At the beginning of extracorporeal life support (ECLS), animals were randomly treated with fingolimod (Group A, n = 30) or saline (Group B, n = 30). Half of the animals in each group (Group A1 and B1, n = 15 each) were sacrificed after 1 h, and the remaining animals (Group A2 and B2) after 24 h of reperfusion. Blood and myocardial tissues were collected for analysis of cardiac features, inflammatory biomarkers, and cell signaling pathways. Results: Treatment with fingolimod resulted in activation of survival pathways resulting into reduced inflammation, myocardial oxidative stress and apoptosis of cardiomyocytes. This led to significant improvement in systolic and diastolic functions of the left ventricle and improved contractility index. Conclusions: Sphingosine1phosphate receptor activation with fingolimod improved cardiac function after cardiac arrest supported with ECLS. Present study findings strongly support a cardioprotective role of fingolimod through sphingosine-1-phosphate receptor activation during reperfusion after circulatory arrest.
- 11 December 2019
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 20 (24) , 6237
Open AccessFingolimod Plays Role in Attenuation of Myocardial Injury Related to Experimental Model of Cardiac Arrest and Extracorporeal Life Support Resuscitation
Background: Sudden cardiac arrest is a major global health concern, and survival of patients with ischemia–reperfusion injury is a leading cause of myocardial dysfunction. The mechanism of this phenomenon is not well understood because of the complex pathophysiological nature of the disease. Aim of the study was to investigate the cardioprotective role of fingolimod in an in vivo model of cardiac arrest and resuscitation. Methods: In this study, an in vivo rat model of cardiac arrest using extracorporeal membrane oxygenation resuscitation monitored by invasive hemodynamic measurement was developed. At the beginning of extracorporeal life support (ECLS), animals were randomly treated with fingolimod (Group A, n = 30) or saline (Group B, n = 30). Half of the animals in each group (Group A1 and B1, n = 15 each) were sacrificed after 1 h, and the remaining animals (Group A2 and B2) after 24 h of reperfusion. Blood and myocardial tissues were collected for analysis of cardiac features, inflammatory biomarkers, and cell signaling pathways. Results: Treatment with fingolimod resulted in activation of survival pathways resulting into reduced inflammation, myocardial oxidative stress and apoptosis of cardiomyocytes. This led to significant improvement in systolic and diastolic functions of the left ventricle and improved contractility index. Conclusions: Sphingosine1phosphate receptor activation with fingolimod improved cardiac function after cardiac arrest supported with ECLS. Present study findings strongly support a cardioprotective role of fingolimod through sphingosine-1-phosphate receptor activation during reperfusion after circulatory arrest.
- 8 October 2012
- Published by BMJ in BMJ Case Reports
- Vol. 2012
Non-compaction of the left ventricle and associated ventricular septal defect
A case report of a 28-year-old patient, who presented with symptoms and signs of congestive heart failure and had clinical signs of ventricular septal defect as well. On further work-up echocardiogram showed non-compaction of the left ventricle with severe left ventricular systolic dysfunction and a ventricular septal defect. He was treated with standard treatment of heart failure and is doing well.
- 8 October 2012
- Published by BMJ in BMJ Case Reports
- Vol. 2012
Non-compaction of the left ventricle and associated ventricular septal defect
A case report of a 28-year-old patient, who presented with symptoms and signs of congestive heart failure and had clinical signs of ventricular septal defect as well. On further work-up echocardiogram showed non-compaction of the left ventricle with severe left ventricular systolic dysfunction and a ventricular septal defect. He was treated with standard treatment of heart failure and is doing well.