The coronavirus disease 2019 (COVID-19) pandemic has resulted in millions of patients infected worldwide and indirectly affecting even more individuals through disruption of daily living. Long-term adverse outcomes have been reported with similar diseases from other coronaviruses, namely Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS). Emerging evidence suggests that COVID-19 adversely affects different systems in the human body. This review summarizes the current evidence on the short-term adverse health outcomes and assesses the risk of potential long-term adverse outcomes of COVID-19. Major adverse outcomes were found to affect different body systems: immune system (including but not limited to Guillain-Barré syndrome and paediatric inflammatory multisystem syndrome), respiratory system (lung fibrosis and pulmonary thromboembolism), cardiovascular system (cardiomyopathy and coagulopathy), neurological system (sensory dysfunction and stroke), as well as cutaneous and gastrointestinal manifestations, impaired hepatic and renal function. Mental health in patients with COVID-19 was also found to be adversely affected. The burden of caring for COVID-19 survivors is likely to be huge. Therefore, it is important for policy makers to develop comprehensive strategies in providing resources and capacity in the healthcare system. Future epidemiological studies are needed to further investigate the long-term impact on COVID-19 survivors.

Hypertension is one of the most important risk factors associated with atrial fibrillation (AF) and increased the risk of cardiovascular events in patients with AF. However, the pathophysiological link between hypertension and AF is unclear. Nevertheless, this can be explained by the hemodynamic changes of the left atrium secondary to long standing hypertension, resulting in elevated left atrium pressure and subsequently left atrial enlargement. Moreover, the activation of renin --angiotensin --aldosterone system (RAAS) activation in patients with hypertension induces left atrial fibrosis and conduction block in the left atrium, resulting in the development of AF. Accordingly, recent studies have shown that effective blockage of RAAS by angiotensin converting enzyme inhibitors or angiotensin receptor antagonist may be effective in both primary and secondary prevention of AF in patients with hypertension, although with controversies. In addition, optimal antithrombotic therapy, blood pressure control as well as rate control for AF are key to the management of patients with AF. 1,2 Both hypertension 3 and AF 4 have increased frequency with the ageing population worldwide, and are associated with increased cardiovascular events. They are important risk factors for stroke, heart failure and overall mortality. 5 --7 On the other hand, hypertension is one of the important risk factors for the occurrence of AF, 8 and increased the risk of stroke and cardiovascular mortality in patients with AF.9,10 Compare with other risk factors for AF, hypertension appears to be responsible for more AF than any other risk factor because of its high prevalence. However, the pathophysiological link between AF and hypertension remains unclear. Moreover, it is also unclear whether treatment of hypertension prevents AF or reduces the risk of AF related complications. The purpose of this article is to review the epidemiology, underlying mechanisms and therapeutic implications of AF in hypertensive patients. A systematic literature search for full-text papers in the English language was performed using MEDLINE, Embase and the Cochrane library through to July 2011. In the search phrases used, the following terms were used: 'atrial fibrillation', 'hypertension', 'epidemiology', 'pathophysiology' and 'treatment'. Papers selected and cited in this review were based on the authors' view on the relevance to the manuscript. In addition, abstracts from international cardiovascular meetings were studied to identify unpublished studies.

The depolarizing membrane ionic current I(h) (also known as I(f), "f" for funny), encoded by the hyperpolarization-activated cyclic-nucleotide-modulated (HCN1-4) channel gene family, was first discovered in the heart over 25 years ago. Later, I(h) was also found in neurons, retina, and taste buds. HCN channels structurally resemble voltage-gated K(+) (Kv) channels but the molecular features underlying their opposite gating behaviors (activation by hyperpolarization rather than depolarization) and non-selective permeation profiles (> or =25 times less selective for K(+) than Kv channels) remain largely unknown. Although I(h) has been functionally linked to biological processes from the autonomous beating of the heart to pain transmission, the underlying mechanistic actions remain largely inferential and, indeed, somewhat controversial due to the slow kinetics and negative operating voltage range relative to those of the bioelectrical events involved (e.g., cardiac pacing). This article reviews the current state of our knowledge in the structure-function properties of HCN channels in the context of their physiological functions and potential HCN-based therapies via bioengineering.

The case is reported of a 75 year old woman who presented with recurrent nocturnal episodes of acute pulmonary oedema. The cause was uncertain as she had normal cardiothoracic ratio on chest radiography and normal left ventricular systolic and diastolic function by transthoracic echocardiogram. Another transthoracic echocardiogram was repeated when she was recumbent for an hour and had a full stomach. It showed a striking finding of severe left atrial compression by an external structure. Computed tomography of the thorax showed an intrathoracic mass behind the left atrium causing external compression of the left atrium suggestive of a sliding hiatus hernia. Cardiac catheterisation confirmed the diagnosis by showing a pronounced rise of pulmonary capillary wedge pressure in the recumbent position compared with the sitting up position.A 75 year old woman presented with recurrent episodes of shortness of breath and chest pain in the previous three months requiring multiple admissions. The diagnosis of acute pulmonary oedema was made but no cause could be found on previous admissions. Her cardiothoracic ratio was normal on chest radiography, her left ventricular function, both systolic and diastolic, were normal by transthoracic echocardiogram. Her symptoms occurred typically at bedtime, especially after a heavy dinner, and were associated with orthopnea, paroxysmal nocturnal dyspnea, and ankle oedema. Physical examination showed regular pulses with a normal blood pressure finding of 124/61 mm Hg. The jugular venous pressure was raised, the heard sounds were normal, and no murmur could be heard. There was bilateral ankle oedema as well as basal crackles heard over both lungs. An electrocardiogram showed normal sinus rhythm without any ischaemic or hypertensive changes. Careful examination of the chest radiograph showed congested lung field with mild bilateral pleural effusion compatible with acute pulmonary oedema. There was also a round shadow behind the heart with an air-fluid level within it. Blood tests including complete blood counts, renal and liver function test, and creatinine kinase activity were within normal limits. Transthoracic echocardiography was repeated when the patient was in the supine position for an hour and had a full stomach. It showed normal left ventricular function but the left atrium was severely compressed by an extrinsic structure confirmed by multiple views (fig 1). Spiral computed tomography of the thorax showed a large hiatus hernia with intrathoracic extension. The hernia was located behind the left atrium causing anterior shift of the heart (fig 2). Subsequently coronary angiography showed normal coronary anatomy. Right heart catheterisation showed that baseline right atrial pressure and pulmonary capillary wedge pressure during prolonged supine positioning were 8 mm Hg and 18 mm Hg respectively. However, after sitting upright for 30 minutes, the right atrial pressure and pulmonary capillary wedge pressure decreased to 5 mm Hg and 6 mm Hg respectively, confirming the diagnosis of s...