Commentary - (2022) Volume 14, Issue 6
Received: 25-May-2022, Manuscript No. ipaom-22-12946; Editor assigned: 28-May-2022, Pre QC No. P-12946; Reviewed: 17-Jun-2022, QC No. Q-12946; Revised: 22-Jun-2022, Manuscript No. R-12946; Published: 30-Jun-2022
Hypertrophic Cardiomyopathy (HCM) is a rather common condition seen by anesthesiologists in the perioperative phase. HCM was thought to be a rare condition fifty years ago. However, our understanding and capacity to diagnose HCM patients has vastly increased in recent years. Patients with HCM have a wide range of genotypic and phenotypic characteristics. A subset of these patients does, in fact, have the HCM genotype but not the manifestation (left ventricular hypertrophy). Pharmacotherapy to control symptoms, implantable cardiac defibrillators to manage malignant arrhythmias, and surgical myectomy and septal ablation to reduce the left ventricular outflow obstruction are all options for these individuals. For the perioperative care of these patients, an accurate diagnosis is critical. Left ventricular hypertrophy, left ventricular outflow tract gradients, systolic and diastolic function, and mitral valve morphology and function are typically used to make the diagnosis. Cardiac magnetic resonance imaging can also be used for diagnosis.
Cardiomyopathy; Macrolides; COVID-19; Pleiotropic data.
Hypertrophic Cardiomyopathy (HCM) was first described in 1868, its functional consequences in 1957, Left Ventricular (LV) asymmetric and especially septal hypertrophy in 1958, and its familial nature in 1960. Hypertrophic Cardiomyopathy (HCM) is characterised by asymmetrical LV thickening without chamber dilation that occurs in the absence of a known aetiology (e.g. aortic valvular stenosis [AS], hypertension), and is accompanied with myocardial fibre disarray:Myocardial cell disarray, in which cells are arranged in a disordered pattern rather than in a typical parallel pattern.Coronary microvasculature failure due to increased wall/ lumen ratio; andremodelling alterations are the key underlying structural abnormalities in HCM.These changes can also affect myocytes, fibroblasts, and the interstitium, and are not restricted to areas of LVH and myocardial remodelling that occur as a compensatory mechanism.
These changes take years to manifest before symptoms appear. Impaired coronary reserve, diastolic dysfunction, supraventricular and ventricular dysrhythmias, and sudden death are all symptoms of HCM patients' disorganised myocyte pattern, increased wall/ lumen ratio of coronaries, and remodelling alterations.Treatment and outcomes— medical and surgicalhe existence and amplitude of LVOTO in HCM patients have been shown to be independent predictors of sudden death and all-cause cardiac mortality.
Given the mechanisms underlying myocardial contraction (calcium ions binding to troponin C and excitation-contraction coupling), as well as the fact that obstruction in HCM is dynamic and lethal dysrhythmias are common, a variety of medical regimens have been used in these patients with the goal of altering the natural history.Through negative inotropy, the purpose of medical care with these medications is to reduce or abolish the LVOT gradient. The majority of medications used to treat symptomatic HCM patients relieve symptoms by lowering or eliminating the LVOT pressure gradient. Because it reduces the dP/dT (change in pressure over time), -adrenergic blockade can help with dyspnea and angina symptoms. This, in turn, causes a decrease in LVOTO.
These drugs help reduce LVOTO during exercise by dampening the sympathetic response, making them useful for managing symptoms and lowering the risk of sudden cardiac death. The medications should be titrated depending on symptom alleviation and an endeavour to avoid any substantial drug-related side effects. Perhexiline, a myocyte energy supplement, has recently been proven to reduce diastolic dysfunction and symptomatology [1-5].
Beyond its antibacterial activities, different antibiotics elicit pleiotropic effects that have the potential to be of great benefit in the clinical treatment of viral infection e.g. COVID-19-induced pneumonia or lung injury preceding event of secondary infections by bacteria. Impairing viral entry, interfering with viral replication, attenuating cytokine storm by reduction of interleukin (IL)-6, IL- 1, tumor necrosis factor (TNF)-α and other combating oxidative stress; explain the potential efficacy of antibiotics in the management of severe cases of viral infections More experimental studies and randomized clinical trials are needed for investigating their role in reducing mortality and improving clinical outcomes.
All authors declare that they have no conflict of interest.
All data generated or analyzed during study are included in this review.
RHT, the corresponding author, has the major contribution in designing, coordinating the duties of each co-author and edited the final version the manuscript. SMMBA, searching in literature about macrolides update pleiotropic activities; HHND, help in designing figures and searching about beta lactam antibiotics; AZIB, help in searching about tetracyclines and fluoroquinolones; MRMT, help in writing manuscript; EMW, help in revising manuscript linguistically. All authors read and approved the final manuscript.
This study was not funded by any specific grant from funding agencies in the public, commercial, or not-forprofit sectors.
None.
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