Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, March 25, 2020

Cardiac injury confers greater mortality in patients with COVID-19

Our fucking failures of stroke associations should be publishing similar research on stroke since we had massive amounts of inflammation in our brains. BUT NOTHING WILL OCCUR! You're screwed.  You will have to do your own research on that issue. You are responsible since no one in stroke is up to the task of solving stroke and associated consequences.

Cardiac injury confers greater mortality in patients with COVID-19 



Among patients with laboratory-confirmed COVID-19 in Wuhan, China, those with cardiac injury had a higher risk for in-hospital mortality than patients without cardiac injury.
According to new research published in JAMA Cardiology, cardiac injury, defined as blood levels of high-sensitivity troponin I above the 99th percentile upper reference limit, appears common among patients hospitalized with COVID-19. Researchers reported cardiac injury occurred in 19.7% of a cohort of 416 consecutive patients.

In-hospital mortality occurred in 51.2% of patients with cardiac injury vs. 4.5% of those without cardiac injury (P < .001), according to the researchers.
Risk for in-hospital death was elevated in patients with cardiac injury and COVID-19, compared with patients with COVID-19 but no cardiac injury, regardless of whether the starting time point was symptom onset (HR = 4.26; 95% CI, 1.92-9.49) or hospital admission (HR = 3.41; 95% CI, 1.62-7.16).
Complication rates
Moreover, patients with cardiac injury experienced higher rates of complications than those without cardiac injury, including acute respiratory distress syndrome (58.5% vs. 14.7%; P < .001), acute kidney injury (8.5% vs. 0.3%; P < .001), electrolyte disturbances (15.9% vs. 5.1%; P = .003), hypoproteinemia (13.4% vs. 4.8%; P = .01) and coagulation disorders (7.3% vs. 1.8%; P = .02).
Researchers also observed that among those with COVID-19, those with cardiac injury more often required noninvasive mechanical ventilation (46.3% vs. 3.9%; P < .001) or invasive mechanical ventilation (22% vs. 4.2%; P < .001) compared with those with no cardiac injury.
“The present study demonstrates the statistically significant association between cardiac injury and mortality in patients with COVID-19,” Shaobo Shi, MD, PhD, of the department of cardiology at Renmin Hospital and the Cardiovascular Research Institute at Wuhan University, China, and colleagues wrote. “Cardiac injury ... was associated with an unexpected high risk of mortality during hospitalization.”
Patient characteristics
Researchers also observed that among patients diagnosed with COVID-19, those with cardiac injury, compared with those without, were more likely to have (P < .001 for all except as noted):
  • advanced age (median age, 74 vs. 60 years);
  • chest pain (13.4% vs. 0.9%);
  • hypertension (59.8% vs. 23.4%);
  • diabetes (24.4% vs 12%; P = .008);
  • CHD (29.3% vs. 6%);
  • cerebrovascular disease (15.9% vs. 2.7%);
  • chronic HF (14.6% vs. 1.5%);
  • chronic obstructive pulmonary disease (7.3% vs. 1.8%; P = .02);
  • cancer (8.5% vs. 0.6%);
  • higher leukocyte counts (median, 9,400 cells/L vs. 5,500 cells/L);
  • higher levels of C-reactive protein (median, 10.2 mg/dL vs. 3.7 mg/dL);
  • higher procalcitonin (median, 0.27 ng/mL vs. 0.06 ng/mL);
  • higher creatinine kinase-MB (median, 3.2 ng/mL vs. 0.9 ng/mL);
  • higher myohemoglobin (median, 128 g/L vs. 39 g/L);
  • higher high-sensitivity troponin I levels (median, 0.19 g/L vs. <0.006 g/L);
  • higher N-terminal pro-B-type natriuretic peptide (median, 1,689 pg/mL vs. 139 pg/mL);
  • more aspartate aminotransferase (median, 40 U/L vs. 29 U/L);
  • higher creatinine levels (median, 1.15 mg/dL vs. 0.64 mg/dL); and
  • a higher proportion of multiple mottling and ground-glass opacity in radiographic findings (64.6% vs. 4.5%).
The retrospective cohort study was conducted from Jan. 20 to Feb. 10 and included 416 consecutive patients (median age, 64 years; 51% women) admitted to Renmin Hospital of Wuhan University with laboratory-confirmed COVID-19.
“The present study lacks evidence from magnetic resonance imaging or echocardiography to determine the features of myocardial injury,” the researchers wrote. “On the basis of the present results of high-sensitivity troponin I and ECG findings in a subset of patients, we can only estimate the severity of cardiac injury. Thus, because of the current limited evidence, the question of whether the SARS-CoV-2 virus can directly injure the heart requires further demonstration.” – by Scott Buzby
Disclosures: The authors report no relevant financial disclosures.

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