Explore chapters and articles related to this topic
Targeted Molecular Imaging in Cardiology
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
NME in cardiology have been directed toward hypertension, blood coagulation and thrombosis. Knock-out of either angiotensin-converting enzyme (ACE) or the angiotensin receptor AT1 results in significant decreases in resting blood pressure in mice. These KO mice be used as a milestone for complete blockade and compared to the effect of ACE inhibitors and AT1 receptor inhibitors (34). KO of the ADP receptor and Factor X have helped to identify the mechanism of action of anti-thrombotic drugs.
Recent advances in patient selection and devices for transcatheter edge-to-edge mitral valve repair in heart failure
Published in Expert Review of Medical Devices, 2020
Martin Orban, Enzo Lüsebrink, Daniel Braun, Thomas J. Stocker, Erik Bagaev, Christian Hagl, Michael Näbauer, Steffen Massberg, Mathias Orban, Jörg Hausleiter
The NNT of COAPT to save one life within 24 months is 5.9, while such numbers are not available for MITRA-Fr due to the neutral study results. Compared to previous studies demonstrating a survival benefit of a novel HF therapy, TMVR is very efficient. For instance, in the PARADIGM-HF (Prospective Comparison of Angiotensin Receptor-Neprilysin Inhibitor with Angiotensin-Converting-Enzyme Inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure Trial) study which showed a survival benefit of the angiotensin receptor-neprilysin inhibitor Sacubitril/Valsartan compared to Enalapril, 36 patients need to be treated over 27 months to save one life [62]. As shown in COAPT, TMVR might be able to stabilize the LV disease and improve prognosis. While the LVEDV increased by 17 mL at 12 months in the OMT group it remained stable in the interventional group (−3.7%). The 6-minute walking distance declines by 60% in the OMT group at 12 months, whereas it remained stable in the interventional group (−2.2%). Concerning symptomatic improvement, the interventional group showed markedly better results than the medical treatment group. Furthermore, quality of life assessed with Kansas City Cardiomyopathy Questionnaire (KCCQ) did not markedly change in the medical treatment group (−3.6%), but it improved by 12.5% in the interventional group.
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
We need to observe patients supported by CF LVADs more carefully and collect more evidence regarding the effects of long-term support in DT. Risk factors for the late decline of renal function should be evaluated using a large database to reveal the likely causes. As we described previously [13], there is a possibility that therapies using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers incidentally prevent inflammatory changes such as periarteritis in the kidneys. Most patients who receive a CF LVAD take these medications as part of a standard therapeutic regimen to suppress the progression of HF. Further research will be needed to determine the effects of angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers on the mechanisms of these pathologic changes. It would also be important to follow the renin activity in patients supported by CF LVAD for the long term. We also need more animal experiments regarding the effects of CF support on end organs. During CF LVAD support, the native heart continues to function and may contribute to cardiac output by ejecting blood through the aortic valve or by increasing the preload pressure to the pump [68]. Either of these possibilities would mean that the CF LVAD support is not completely nonpulsatile, even in animal experiments. We can create a completely nonpulsatile flow condition by using our CF TAH and could examine the effects of CF support more precisely [69]. We are planning future animal experiments to evaluate the effects of the CF TAH with completely nonpulsatile settings.
The influence of climate change on human cardiovascular function
Published in Archives of Environmental & Occupational Health, 2020
Milos Gostimirovic, Radmila Novakovic, Jovana Rajkovic, Vladimir Djokic, Dusko Terzic, Svetozar Putnik, Ljiljana Gojkovic-Bukarica
Not only drug effects, but all pharmacokinetic processes, including route of administration can be affected by high environmental temperature. Studies dealing with the effects of external heating on the absorption and elimination of some orally administered drugs have shown minor changes in plasma drug concentrations, in contrast to systemic absorption of drugs which were taken transdermal or subcutaneously. Drug distribution can be slightly influenced by changes in blood volume due to excessive dehydration, which in turn reduces Vd of non-highly lipid-soluble drugs. It is known that enzymes lose their morphological stability and activity at higher temperatures. Hepatic enzyme activity contributes to the hepatic metabolism of high-extraction drugs, and an increase in the ambient temperature may be reflected as enhanced enzyme-catalysed reactions, reducing hepatic clearance of such drugs At high temperatures, renal blood flow is decreased which together with dehydration and hormonal changes reduce urine output and limit drug elimination. Taking antihypertensive medications augment water lose and dehydration and lead to renal damage, possibly culminating to the end stage kidney disease, which can increase Emergency Department(ED) visits and hospital admissions.26 Additionally, patients who chronically use combination of thiazide and ACE-inhibitors/(angiotensin receptor blockers)ARBs may lead to increase the in serum creatinine, predisposing to acute kidney failure via volume depletion, decreased renal perfusion and lightning the response of the renin-angiotensin system in elderly patients, especially if earlier kidney damage is present.27