Document reviewers: Hind Beheiry (Sudan), Irina Chazova (Russia), Albertino Damasceno (Mozambique), Anna Dominiczak (UK), Anastase Dzudie (Cameroon), Stephen Harrap (Australia), Hiroshi Itoh (Japan), Tazeen Jafar (Singapore), Marc Jaffe (USA), Patricio Jaramillo-Lopez (Colombia), Kazuomi Kario (Japan), Giuseppe Mancia (Italy), Ana Mocumbi (Mozambique), Sanjeevi N.Narasingan (India), Elijah Ogola (Kenya), Srinath Reddy (India), Ernesto Schiffrin (Canada), Ann Soenarta (Indonesia), Rhian Touyz (UK), Yudah Turana (Indonesia), Michael Weber (USA), Paul Whelton (USA), Xin Hua Zhang, (Australia), Yuqing Zhang (China).

https://repository.nwu.ac.za/bitstream/10394/34842/1/2020%20International%20Society%20of%20Hypertension.pdf

2020 International Society of Hypertension global hypertension practice guidelines

We tested the usefulness of aspirin (325 mg twice daily), heparin (1000 units per hour by intravenous infusion), and a combination of the two in the early management of acute unstable angina pectoris in a double-blind, randomized, placebo-controlled trial involving 479 patients. The patients entered the study as soon as possible after hospital admission (at a mean [+/- SD] of 7.9 +/- 8.0 hours after the last episode of pain), and the study was ended after 6 +/- 3 days, when definitive therapy had been selected. Major end points--refractory angina, myocardial infarction, and death--occurred in 23, 12, and 1.7 percent of the 118 patients receiving placebo, respectively. Heparin was associated with a decrease in the occurrence of refractory angina (P = 0.002). The incidence of myocardial infarction was significantly reduced in the groups receiving aspirin (3 percent; P = 0.01), heparin (0.8 percent; P less than 0.001), and aspirin plus heparin (1.6 percent, P = 0.003), and no deaths occurred in these groups. There were too few deaths overall to permit evaluation of the effect of treatment on this end point. The combination of aspirin and heparin had no greater protective effect than heparin alone but was associated with slightly more serious bleeding (3.3 vs. 1.7 percent). We conclude that in the acute phase of unstable angina, either aspirin or heparin treatment is associated with a reduced incidence of myocardial infarction, and there is a trend favoring heparin over aspirin. Heparin treatment is also associated with a reduced incidence of refractory angina.

Aspirin, heparin, or both to treat acute unstable angina

Objective: To determine whether vegetations visualized on two-dimensional echocardiography are an independent risk factor for the development of subsequent emboli in patients with infective endocar...

Emboli in Infective Endocarditis: The Prognostic Value of Echocardiography

DOCUMENT REVIEWERS\nHind Beheiry (Sudan), Irina Chazova (Russia), Albertino Damasceno (Mozambique), Anna Dominiczak (UK), Anastase Dzudie (Cameroon), Stephen Harrap (Australia), Hiroshi Itoh (Japan), Tazeen Jafar (Singapore), Marc Jaffe (USA), Patricio Jaramillo-Lopez (Colombia), Kazuomi Kario (Japan), Giuseppe Mancia (Italy), Ana Mocumbi (Mozambique), Sanjeevi N.Narasingan (India), Elijah Ogola (Kenya), Srinath Reddy (India), Ernesto Schiffrin (Canada), Ann Soenarta (Indonesia), Rhian Touyz (UK), Yudah Turana (Indonesia), Michael Weber (USA), Paul Whelton (USA), Xin Hua Zhang, (Australia), Yuqing Zhang (China).

/pdf/2020-international-society-of-hypertension-global-3pxw0w3zuf.pdf

2020 International Society of Hypertension global hypertension practice guidelines.

http://www.antimicrobe.org/Chang%20Endo%20Medicine%202003.pdf

A prospective multicenter study of Staphylococcus aureus bacteremia: incidence of endocarditis, risk factors for mortality, and clinical impact of methicillin resistance.

COVID-19 infection and cardiac arrhythmias.

Coronavirus-2019 (COVID-19) predisposes patients to arterial and venous thrombosis commonly complicating the clinical course of hospitalized patients and attributed to the inflammatory state, endothelial dysfunction, platelet activation and blood stasis. This viral coagulopathy may occur despite thromboprophylaxis and raises mortality; the risk appears highest among critically ill inpatients monitored in the intensive care unit. The prevalence of venous thromboembolism in COVID-19 patients has been reported to reach ∼10-35%, while autopsies raise it to nearly 60%. The most common thrombotic complication is pulmonary embolism, which though may occur in the absence of a recognizable deep venous thrombosis and may be due to pulmonary arterial thrombosis rather than embolism, resulting in thrombotic occlusion of small- to mid-sized pulmonary arteries and subsequent infarction of lung parenchyma. This micro-thrombotic pattern seems more specific for COVID-19 and is associated with an intense immuno-inflammatory reaction that results in diffuse occlusive thrombotic micro-angiopathy with alveolar damage and vascular angiogenesis. Furthermore, thrombosis has also been observed in various arterial sites, including coronary, cerebral and peripheral arteries. Biomarkers related to coagulation, platelet activation and inflammation have been suggested as useful diagnostic and prognostic tools for COVID-19-associated coagulopathy; among them, D-dimer remains a key biomarker employed in clinical practice. Various medical societies have issued guidelines or consensus statements regarding thromboprophylaxis and treatment of these thrombotic complications specifically adapted to COVID-19 patients. All these issues are detailed in this review, data from meta-analyses and current guidelines are tabulated, while the relevant mechanisms of this virus-associated coagulopathy are pictorially illustrated.

https://journals.sagepub.com/doi/pdf/10.1177/1074248420958973

COVID-19 Infection: Viral Macro- and Micro-Vascular Coagulopathy and Thromboembolism/Prophylactic and Therapeutic Management.

Sudden unexpected death in epilepsy (SUDEP) is the major cause of epilepsy-related premature mortality which targets preferentially younger people. Its etiology remains unknown. Several risk factors have been identified with generalized tonic-clonic seizures as the most important one; seizure control remains the most effective measure of prevention. Although some cases may be attributable to cardiac causes, mainly undiagnosed cardiac channelopathies, the majority appear linked to epilepsy-related disruption of the functional connectivity of certain brain structures associated with the central autonomic control of cardio-respiratory function (neuro-cardio-respiratory connection). Obtaining further data on its pathophysiologic mechanisms is a cardinal step towards preventing and reducing the incidence of SUDEP. Neuroimaging and molecular genetic studies may provide insights into the causes of SUDEP and identify potential biomarkers for risk stratification of patients susceptible to SUDEP. These issues are herein reviewed with emphasis placed on the neuro-cardio-respiratory functions affected by epilepsy and their genetic control and influences.

Sudden unexpected death in epilepsy: The neuro-cardio-respiratory connection

Mitochondria provide energy to the cell during aerobic respiration by supplying ~95% of the adenosine triphosphate (ATP) molecules via oxidative phosphorylation. These organelles have various other functions, all carried out by numerous proteins, with the majority of them being encoded by nuclear DNA (nDNA). Mitochondria occupy ~1/3 of the volume of myocardial cells in adults, and function at levels of high-efficiency to promptly meet the energy requirements of the myocardial contractile units. Mitochondria have their own DNA (mtDNA), which contains 37 genes and is maternally inherited. Over the last several years, a variety of functions of these organelles have been discovered and this has led to a growing interest in their involvement in various diseases, including cardiovascular (CV) diseases. Mitochondrial dysfunction relates to the status where mitochondria cannot meet the demands of a cell for ATP and there is an enhanced formation of reactive-oxygen species. This dysfunction may occur as a result of mtDNA and/or nDNA mutations, but also as a response to aging and various disease and environmental stresses, leading to the development of cardiomyopathies and other CV diseases. Designing mitochondria-targeted therapeutic strategies aiming to maintain or restore mitochondrial function has been a great challenge as a result of variable responses according to the etiology of the disorder. There have been several preclinical data on such therapies, but clinical studies are scarce. A major challenge relates to the techniques needed to eclectically deliver the therapeutic agents to cardiac tissues and to damaged mitochondria for successful clinical outcomes. All these issues and progress made over the last several years are herein reviewed.

Mitochondrial dysfunction in cardiovascular disease: Current status of translational research/clinical and therapeutic implications

• Thirty-four drug addicts with endocarditis were studied to evaluate the prognostic significance of vegetation size and its short-term changes, as determined by two-dimensional echocardiography. Among 43 episodes of endocarditis, vegetations were detected in 27 (63%), confined to the tricuspid valve in 20 patients, mitral valve in one, aortic valve in two, and both tricuspid and mitral valves in four. All vegetations were large (≥1 cm) (mean maximal dimension, 1.7±0.5 cm). Medical cure was achieved in all 16 patients without vegetations and in 18 (90%) of 20 patients with tricuspid valve vegetations. One patient with tricuspid vegetation and polymicrobial infection died of respiratory failure. Surgery was required for one patient with tricuspid vegetation, all three patients with isolated left-sided endocarditis, and two of four patients with multivalve involvement. Short-term changes of tricuspid valve vegetations during therapy (one to eight weeks) did not correlate with clinical outcome. Although large tricuspid vegetations may occasionally identify a subset at risk for complications, most patients with isolated tricuspid valve endocarditis have a benign prognosis. ( Arch Intern Med 1988;148:2461-2465)

Helen Melita

Papers

COVID-19 infection and cardiac arrhythmias.

COVID-19 Infection: Viral Macro- and Micro-Vascular Coagulopathy and Thromboembolism/Prophylactic and Therapeutic Management.

Sudden unexpected death in epilepsy: The neuro-cardio-respiratory connection

Mitochondrial dysfunction in cardiovascular disease: Current status of translational research/clinical and therapeutic implications

Echocardiographic and Clinical Correlates in Drug Addicts With Infective Endocarditis: Implications of Vegetation Size