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1.
Cureus ; 15(2): e35557, 2023 Feb.
Article in English | MEDLINE | ID: mdl-37007363

ABSTRACT

Tachy-brady syndrome is the result of sinus node dysfunction (SND), an electrocardiographic phenomenon caused by defective pacemaker functioning that leads to alternating arrhythmias. We present a case of a 73-year-old male with multiple mental health and medical comorbidities who was admitted to the inpatient floor for catatonia, paranoid delusions, refusal to eat, inability to cooperate with activities of daily life, and generalized weakness. Upon admission, a 12-lead electrocardiogram (ECG) showed an episode of atrial fibrillation with a ventricular rate of 64 beats per minute (bpm). During hospitalization, telemetry recorded a variety of arrhythmias such as ventricular bigeminy, atrial fibrillation, supraventricular tachycardia (SVT), multifocal atrial contractions, and sinus bradycardia. Each episode spontaneously reverted and the patient remained asymptomatic throughout these arrhythmic changes. These frequently fluctuating arrhythmias on resting ECG confirmed the diagnosis of tachycardia-bradycardia syndrome, also known as tachy-brady syndrome. Medical intervention, especially for cardiac arrhythmias, in patients with paranoid and catatonic schizophrenia can be challenging, as they might not share their symptoms. Additionally, certain psychotropic medications can also cause cardiac arrhythmias and must be carefully evaluated. The decision was made to start the patient on a beta-blocker and direct oral anticoagulation for reducing the risk of thromboembolic events. Due to an unsatisfactory response to drug therapy alone, the patient qualified as a candidate for definitive treatment with an implantable dual-chamber pacemaker. Our patient had a dual-chamber pacemaker implanted to prevent bradyarrhythmias and continued oral beta-blockers to prevent tachyarrhythmias.

2.
Cureus ; 15(1): e33265, 2023 Jan.
Article in English | MEDLINE | ID: mdl-36741673

ABSTRACT

This study was conducted to test the hypothesis that platelet-rich plasma (PRP) therapy in chronic respiratory disease patients will cause lung regeneration, thereby slowing the progression of the disease. We performed a search to obtain pertinent articles on the following electronic databases: Google Scholar, PubMed, NCBI, Medscape, and clinicaltrials.gov. Keywords used during in search included "Platelet Rich Plasma" AND "Chronic Respiratory Disease" AND/OR "Chronic Obstructive Pulmonary Disease". A total of 15 articles were chosen for this paper, published from 2011 to 2021, and included case series, lab studies, animal studies, cohort studies, and clinical trials. All statistical data were considered significant if the p-value was less than 5%, or 0.05. Our findings confirmed that PRP therapy successfully caused anti-inflammatory effects and acceleration of tissue regeneration, resulting in improved lung function. This, in turn, slowed the progression of the disease and led to an improved quality of life. Not all chronic respiratory disease patients present in the same manner, but the connecting link is the damaged tissue of the lungs, causing issues with the functionality of the lungs. By adjunctively treating patients with PRP, the high concentration of platelets and their secreted growth factors can help induce an acceleration of healing and regeneration of pulmonary tissue. This, in turn, can slow the progression of the disease, which could lower the overall mortality rate in chronic respiratory disease patients. More studies should be conducted on this topic, specifically large, double-blinded, randomized human trials with controls, to further assess the efficacy and beneficial effects of PRP treatment on the lungs.

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