Techycardia induced cardiomyopathy
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1. The pathophysiology of tachycardia-induced cardiomyopathy (TIC) occurs over three phases: compensatory, left ventricular dysfunction, and left ventricular failure phases. 2. During all three phases, there is left ventricular remodeling and failure, neurohormonal activation, defects in calcium ion handling, and extracellular matrix remodeling. 3. In the later phases, left ventricular dilation and declining ejection fraction occur, leading to heart failure as pathological changes develop.
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We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.Cell Therapy Expansion and Challenges in Autoimmune Disease
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Techycardia induced cardiomyopathy
- 1. Name of the School: SMAS Course Code: BCVT2004 Course Name: CARDIOPATHOPHYSIOLOGY-I Student Name: FATIMA ZEHRA Program Name: B.Sc CVT Admission Number: 21SMAS1040048 PATHOPHYSIOLOGY OF TACHYCARDIA INDUCED CARDIOMYOPATHY.
- 2. The Pathophysiology of TIC takes approximately three weeks divided into three phases: 1- Compensatory phase- 7 days. 2- LV dysfunction phase- 1 to 3 weeks. 3- LV failure phase- > 3 weeks. PATHOPHYSIOLOGY
- 4. There are some events happening during all the 3 phases:- - LV remodeling and LV failure. - Neurohormonal activation. - Defect in Ca2+ ion handling. - Extra celullar matrix remodelling.
- 5. -In developmental stages of TIC (3-7 days) rapid cardiac pacing by dialatation of LV. -Declining LV ejection fraction however, these early changes are not sufficient to cause an interference to either CO or systamic perfusion pressure. -by 2nd week LV dilates -LVEF falls increase in central venous pressure and pulmonary capillary wedge pressure (an integrated measurement of the compliance of the left side of the heart and the pulmonary circulation), and systemic vascular resistance ( the resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature.) -these pathological changes causes the development of HF -LV dilatation and dysfunction causes a decline in intrinsic myocardial contractility. LV remodelling and LV failure
- 6. -The ANP and BNP increases in early stages but iventually decreases because of suppressed synthesis. *In neurohormaonal activation machanism:- Activation of sympathatic pathway ↓ Norepinephrine spillover ↓ Progressive LV dysfunction ↓ Chronic rapid pacing activates the renin angiotensin aldosteron system (RAAS) NEUROHORMONAL ACTIVATION
- 8. Defect in Ca2+ ion handling Under Healthy Condition:- Elevated contraction frequency creates a +ve force frequency relationship( the phenomenon in which the force produced by a muscle increases with the frequency of activation, ) characterised by progressive increase in myocardial contraction resulting from changes in Ca2+ ions handling and in myocardial response to Ca2+. Under ITC condition:- positive force frequensy relationship is weaker accompanied by prolonged myocardial Ca2+ transient and defect in Ca2+ cyding.
- 9. Defect in Ca2+ ion handling Changes in Ca2+ handling leads to impared excitation contraction coupling process, which in turn results into impared myocytes contractility and isotropic responsiveness. These changes have been observed during the development of ITC.
- 11. Extracelular matrix remodeling • The loss of normal fibrillary collagen contented and distribution , causes alternation in myocytes supports and alligment in LV wall accompanied by diminished capacity of myocyte to bind in the extracellular matrix