Archive for the ‘Heart Issues’ Category

Vaccine-Induced Thrombocytopenia With Severe Headache – Why Lyme/MSIDS Patients Should Care

Vaccine-Induced Thrombocytopenia with Severe Headache

To the Editor:

Vaccine-induced immune thrombotic thrombocytopenia (VITT), a serious adverse event after vaccination with ChAdOx1 nCoV-19 (AstraZeneca) or Ad26.COV2.S (Johnson & Johnson–Janssen), is caused by platelet factor 4 (PF4)–dependent, platelet-activating antibodies.1-3 High-dose immune globulins and anticoagulation are the main treatments.4,5 In this report, we present evidence that vaccine-induced thrombocytopenia (VIT) without associated cerebral venous sinus thrombosis (CVST) or other thromboses and with severe headache as the heraldic symptom may precede VITT (“pre-VITT syndrome”).

Eleven patients presented with severe headache in the absence of CVST 5 to 18 days after ChAdOx1 nCoV-19 vaccination.

  • All the patients had thrombocytopenia (low platelets in the blood which can cause hemorrhaging)
  • high d-dimer levels (a test to detect blood clots – a high level indicates clot formation and breakdown in the body)
  • high levels of anti–PF4–heparin IgG antibodies
  • during follow-up, intracranial hemorrhage occurred in three patients (Patients 1, 2, and 3), with radiologic evidence of new CVST in Patients 2 and 3 (Figure 1, and Table S1 in the Supplementary Appendix, available with the full text of this letter at
  • Only two patients (Patients 2 and 4) were initially admitted with conditions that met the criteria for VITT; both patients had pulmonary embolism, and additional splanchnic vein thrombosis was present in Patient 2.

In Patient 2, anticoagulation treatment had been initiated several days earlier for pulmonary embolism (without diagnosis of VITT) but was stopped after the onset of headache, shortly before CVST developed.

  • In two patients (Patients 1 and 3), peripheral thromboses were eventually identified during follow-up.

Thrombotic complications did not develop in seven of the patients (Patients 5 through 11); all but one of these patients received high-dose immune globulin, glucocorticoids, or therapeutic-dose anticoagulation within 5 days after headache onset. In contrast, in all four patients with subsequent thrombosis (Patients 1 through 4), therapeutic-dose anticoagulation either was not started until 6 to 9 days after headache onset or was stopped prematurely before the development of CVST.

Although the combination of thrombocytopenia and severe headache due to CVST has been recognized as the typical presentation of VITT,1,2 the experience with these 11 patients suggests that VIT with severe headache, elevated d-dimer levels, and strongly positive results on anti–PF4–heparin IgG enzyme-linked immunosorbent assay may precede VITT.

Our findings have immediate implications for clinical practice: in this pre-VITT syndrome, severe headache may not develop as a symptom secondary to CVST but instead may precede CVST by several days, potentially in association with microthrombosis in smaller cortical veins.

Consequently, patients who present with severe headache 5 to 20 days after adenovirus vector vaccination against coronavirus disease 2019 should undergo immediate testing for thrombocytopenia and d-dimer levels and, if available, testing for anti–PF4–heparin IgG antibodies.

When these antibodies are present at high titers, patients are at imminent risk for CVST, and it is likely that this condition can be prevented with immediate treatment, such as with intravenous immune globulin. The decision to initiate therapeutic-dose anticoagulation is a difficult one; the risk of emerging thrombosis, including CVST, has to be balanced against the risk of intracranial hemorrhage on an individual basis (e.g., with consideration of platelet count and fibrinogen levels).

Farid Salih, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Linda Schönborn, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Siegfried Kohler, M.D., Christiana Franke, M.D., Martin Möckel, M.D., Thomas Dörner, M.D., Hans C. Bauknecht, M.D., Christian Pille, M.D., Jan A. Graw, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Angelika Alonso, M.D.
University Hospital of Mannheim, Mannheim, Germany

Johann Pelz, M.D.
University Hospital of Leipzig, Leipzig, Germany

Hauke Schneider, M.D., Antonios Bayas, M.D., Monika Christ, M.D.
University Hospital of Augsburg, Augsburg, Germany

Joji B. Kuramatsu, M.D.
University Hospital of Erlangen, Erlangen, Germany

Thomas Thiele, M.D., Andreas Greinacher, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Matthias Endres, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Supported by Deutsche Forschungsgemeinschaft project number 374031971–TRR 240 (to Prof. Greinacher) and EXC-2049–390688087 NeuroCure under the German Excellence Strategy (to Prof. Endres) and by the Domagk-Programm of the Universitätsmedizin Greifswald (to Dr. Schönborn).

Disclosure forms provided by the authors are available with the full text of this letter at

This letter was published on September 15, 2021, at

Profs. Greinacher and Endres contributed equally to this letter.



Both Thrombocytopenia and severe headaches are common with Lyme/MSIDS patients.

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function.

Hopefully it’s clear that a Lyme/MSIDS patient getting a COVID shot could be diagnosed with thrombocytopenia that either already exists or worsens after the injection.  Treating the underlying infection is imperative but won’t be considered by mainstream medicine.

For more:

Go here for the latest VAERS data and the mounting list of adverse reactions and deaths.

Myocarditis After COVID-19 mRNA Shots But Just Mask Up & Shut Up

Myocarditis after Covid-19 mRNA Vaccination

This letter was published on August 18, 2021, at


The Centers for Disease Control and Prevention recently reported cases of myocarditis and pericarditis in the United States after coronavirus disease 2019 (Covid-19) messenger RNA (mRNA) vaccination.1 In recently published reports, diagnosis of myocarditis was made with the use of noninvasive imaging and routine laboratory testing.2-5 Here, we report two cases of histologically confirmed myocarditis after Covid-19 mRNA vaccination.

Figure 1. Histopathological Findings from Endomyocardial Biopsy and Autopsy.

Patient 1, a 45-year-old woman without a viral prodrome, presented with dyspnea and dizziness 10 days after BNT162b2 vaccination (first dose). A nasopharyngeal viral panel was negative for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza A and B, enteroviruses, and adenovirus (Table S1 in the Supplementary Appendix, available with the full text of this letter at A serum polymerase-chain-reaction (PCR) assay and serologic tests showed no evidence of active parvovirus, enterovirus, human immunodeficiency virus, or infection with SARS-CoV-2. At presentation, she had tachycardia; ST-segment depression detected on electrocardiography, which was most prominent in the lateral leads (Fig. S1); and a troponin I level of 6.14 ng per milliliter (reference range, 0 to 0.30). A transthoracic echocardiogram showed severe global left ventricular systolic dysfunction (ejection fraction, 15 to 20%) and normal left ventricular dimensions. Right heart catheterization revealed elevated right- and left-sided filling pressures and a cardiac index of 1.66 liters per minute per square meter of body-surface area as measured by the Fick method. Coronary angiography revealed no obstructive coronary artery disease. An endomyocardial biopsy specimen showed an inflammatory infiltrate predominantly composed of T-cells and macrophages, admixed with eosinophils, B cells, and plasma cells (Figure 1A and Figs. S2 through S4). She received inotropic support, intravenous diuretics, methylprednisolone (1 g daily for 3 days), and, eventually, guideline-directed medical therapy for heart failure (lisinopril, spironolactone, and metoprolol succinate). Seven days after presentation, her ejection fraction was 60%, and she was discharged home.

Patient 2, a 42-year-old man, presented with dyspnea and chest pain 2 weeks after mRNA-1273 vaccination (second dose). He did not report a viral prodrome, and a PCR test was negative for SARS-CoV-2 (Table S1). He had tachycardia and a fever, and his electrocardiogram showed diffuse ST-segment elevation (Fig. S1). A transthoracic echocardiogram showed global biventricular dysfunction (ejection fraction, 15%), normal ventricular dimensions, and left ventricular hypertrophy. Coronary angiography revealed no coronary artery disease. Cardiogenic shock developed in the patient, and he died 3 days after presentation. An autopsy revealed biventricular myocarditis (Figure 1B and Figs. S5 and S6). An inflammatory infiltrate admixed with macrophages, T-cells, eosinophils, and B cells was observed, a finding similar to that in Patient 1.

In these two adult cases of histologically confirmed, fulminant myocarditis that had developed within 2 weeks after Covid-19 vaccination, a direct causal relationship cannot be definitively established because we did not perform testing for viral genomes or autoantibodies in the tissue specimens. However, no other causes were identified by PCR assay or serologic examination.

Amanda K. Verma, M.D.
Kory J. Lavine, M.D., Ph.D.
Chieh-Yu Lin, M.D., Ph.D.
Washington University School of Medicine, St. Louis, MO

________________________  4 Min. Video Here

The HighWire with Del Bigtree
Published Aug. 16, 2021


Entering the ridiculous, public health officials are now asking people not to talk to stop the Covid virus. Jefferey Jaxen dives into the science behind the latest Covid mitigation suggestion.



The video is revealing on many fronts:

  • Propaganda is alive and well.
  • The paper “Viral Load of SARS-CoV-2 in Respiratory Aerosols Emitted By COVID-19 Patients While Breathing, Talking, and Singing,” has numerous disclaimers in fine print, namely, that they couldn’t mechanically retrieve and isolate a viable virus from ambient air in the vicinity of patients.  Well, that’s inconvenient.
  • This study demonstrates perfectly the hypocrisy of our corrupt public health ‘authorities’ in that they demand perfectly done randomized, controlled trials on thousands of patients to approve COVID treatments, completely ignoring clinical results, but will accept and propagate poorly done science that pushes their continued fear narrative that lines their pockets. And even when there properly done RCTs they ignore them and then go on a smear campaign to malign them, and implement bandwagon to make the public believe their accepted narrative.
  • This duplicity has been going on in Lyme-land for over 40 years and continues today.  Hopefully people are waking up to it.

Vaccine-Induced Thrombocytopenia & Thrombosis

Clinical Features of Vaccine-Induced Immune Thrombocytopenia and Thrombosis

List of authors.

  • Sue Pavord, F.R.C.Path., 
  • Marie Scully, M.D., 
  • Beverley J. Hunt, M.D., 
  • William Lester, M.D., 
  • Catherine Bagot, M.D., 
  • Brian Craven, M.B., B.Ch., 
  • Alex Rampotas, M.R.C.P., 
  • Gareth Ambler, Ph.D., 
  • and Mike Makris, M.D.



Vaccine-induced immune thrombocytopenia and thrombosis (VITT) is a new syndrome associated with the ChAdOx1 nCoV-19 adenoviral vector vaccine against severe acute respiratory syndrome coronavirus 2. Data are lacking on the clinical features of and the prognostic criteria for this disorder.


We conducted a prospective cohort study involving patients with suspected VITT who presented to hospitals in the United Kingdom between March 22 and June 6, 2021. Data were collected with the use of an anonymized electronic form, and cases were identified as definite or probable VITT according to prespecified criteria. Baseline characteristics and clinicopathological features of the patients, risk factors, treatment, and markers of poor prognosis were determined.


Among 294 patients who were evaluated, we identified:

  • 170 definite cases of VITT
  • 50 probable cases of VITT
  • All the patients had received the first dose of ChAdOx1 nCoV-19 vaccine and presented 5 to 48 days (median, 14) after vaccination. The age range was 18 to 79 years (median, 48), with no sex preponderance and no identifiable medical risk factors
  • Overall mortality was 22%
  • The odds of death increased by a factor of
    • 2.7 (95% confidence interval [CI], 1.4 to 5.2) among patients with cerebral venous sinus thrombosis
    • 1.7 (95% CI, 1.3 to 2.3) for every 50% decrease in the baseline platelet count
    • 1.2 (95% CI, 1.0 to 1.3) for every increase of 10,000 fibrinogen-equivalent units in the baseline d-dimer level
    • 1.7 (95% CI, 1.1 to 2.5) for every 50% decrease in the baseline fibrinogen level
    • Multivariate analysis identified the baseline platelet count and the presence of intracranial hemorrhage as being independently associated with death
    • observed mortality was 73% among patients with platelet counts below 30,000 per cubic millimeter and intracranial hemorrhage

The high mortality associated with VITT was highest among patients with a low platelet count and intracranial hemorrhage. Treatment remains uncertain, but identification of prognostic markers may help guide effective management. (Funded by the Oxford University Hospitals NHS Foundation Trust.)



The numbers don’t lie.  

A majority of these “vaccinated” patients had VITT which explains what is happening in reality – blood clotting issues.  

  • We’ve been warned by a Canadian doctor doing D-dimer tests on his “vaccinated” patients that 62% show microscopic blood clotting.
  • A pathologist also states these injections cause severe inflammation due to the “spike protein” which is a dangerous toxin that crosses the blood-brain barrier and disrupts blood vessels throughout the body and brain.  He also reiterates that these injections are not “vaccines.”

Please notice the overall mortality of 22% and significant increased odds of death on these fully “vaccinated” individuals that have been told ad nauseam that these injections will be protective and keep you from hospitalization and death.

For a mounting list of adverse reactions and death (with many examples of blood clotting & cardiovascular issues – even in young people):

Lyme Carditis 2021 Update

Adrian Baranchuk, MD, Guest Blog – Lyme Carditis 2021 Update

LDA Guest Blogger


Adrian Baranchuk MD, FACC, FRCPC, FCCS, FSIAC is Professor of Medicine at Queen’s University, Kingston, Ontario, Canada. He is Editor-in-chief, Journal of Electrocardiology; Vice President, International Society of Holter and Non-Invasive Electrocardiology (ISHNE); Secretary, Interamerican Society of Cardiology (SIAC); Co-Director, ECG University; Past President, International Society of Electrocardiology (ISE); and Director, NET-Heart Project (Neglected Tropical Diseases and other Infectious Diseases affecting the Heart).

Lyme Carditis: Update 2021. An Evasive Diagnosis in the Time of COVID-19

Adrian Baranchuk MD, FACC, FRCPC, FCCS, FSIAC; Chang (Nancy) Wang MSc (c), MD
Department of Medicine, Kingston Health Science Center, Kingston, Ontario, Canada

Lyme disease (LD) is a tick-borne bacterial infection caused by Borrelia burgdorferi. Lyme carditis (LC) is an early-disseminated manifestation of LD, most commonly manifesting as a complete “shut-down” of the electrical system (high-degree atrioventricular block (AVB)) that can evolve rapidly over minutes, hours, or days producing severe symptoms like fainting, palpitations, shortness of breath, extreme dizziness, or sudden death (1-2).

Other cardiovascular manifestations include alterations of the “motor” of the heart (sinus node disease) (3), a disorganization of the cardiac rhythm that increases the risk of stroke (atrial fibrillation) (2), lesion in the distal cables of the heart (bundle branch blocks) (4), and different degrees of inflammation of the layers of the cardiac walls (myocarditis, pericarditis, and endocarditis) (2). Some of these manifestations could be so severe that a total dysfunction of the cardiac function occurs in a matter of hours, and the patient may die even if admitted to the best ICU in the world.

The initial symptoms of LD can be mistaken by other common infections or allergic reactions. Delayed diagnosis is one of the most important risk factors to serious LD presentations including LC in all its forms. The good news is that prompt diagnosis and appropriate antibiotic therapy links to a much better prognosis. In addition, we now know that when appropriately treated with antibiotics according to guidelines (2); there is no evidence of residual disease in the heart (5).

Most conduction abnormalities caused by LC resolve with appropriate antibiotic therapy (2).

The current COVID-19 pandemic is posing a new challenge in the diagnosis of LD. There are lots of overlapping symptoms such as: fever, malaise, generalized pain, lack of energy, etc. During these times, one would advise on ruling out COVID-19 first before embarking on any other test. However, what could we recommend in terms of confirming or ruling out LD, specifically during these challenging times?

Learning how to recognize the many presentations of LD from a clinical point of view has been published several times. It is especially important to ask about outdoor activities, history of tick bites, tick removal and dermatological rashes (remember that the classic “bull eye” is only present in about 40% of cases). Extensive dermatologic examination may be necessary. Residence in an endemic region for LD is essential for risk stratification, as these recommendations should be encouraged in all ED and family doctor offices in areas of high prevalence.

Once the diagnosis is suspected, specific interrogation should be directed to cardiovascular symptoms such as: dizziness, palpitations, fainting or near fainting, chest pain and shortness of breath. If the patient recognizes any of these symptoms, along with any other factors suggesting LD, a 12-lead ECG (the simple and unexpensive electrocardiogram) should be performed (2). Any evidence of electrical disturbance should prompt admission in hospital for a course of IV antibiotics while waiting the results of serological tests.

On the other hand, in patients presenting with unexpected high-degree AV block, clinical suspicion for LC can be assessed using the validated risk score called SILC (Suspicious Index in Lyme carditis) (6) where the acronym COSTAR(Constitutional symptoms, Outdoor activities/endemic region, Sex male, Tick bite, Age > 50, Rash) may help in determining the risk of presenting early disseminated LC.

In summary, use your clinical tools to suspect LD in the context of COVID-19 pandemic, order serological tests when appropriate, and remember to check for cardiovascular complications with a history, physical, and ECG. If evidence of LC, admit the patient to hospital with continuous cardiac monitoring and appropriate IV antibiotics. Decision for permanent pacemaker implantation should wait until completion of antibiotics as heart block in LC is often reversible. Most patients maintain normal rhythm on long-term follow-up. Avoiding unnecessary implants is crucial as most of these patients are young and active individuals.

1. Wan D, Blakely C, Branscombe P, Suarez-Fuster L, Glover B, Baranchuk A. Lyme Carditis and High-degree Atrioventricular Block. Am J Cardiol 2018; 26(5): 233-239
2. Yeung C, Baranchuk A. Diagnosis and Treatment of Lyme Carditis. J Am Coll Cardiol 2019; 73(6): 717-726
3. Gazendam N, Yeung C, Baranchuk A. Lyme carditis presenting as sick sinus syndrome. J Electrocardiol 2020; 59: 65-67
4. Maxwell N, Dryer M, Baranchuk A, Vinocur M. Phase 4 Block of the Right Bundle Branch Suggesting His-Purkinje System Involvement in Lyme Carditis. HeartRhythm Case Reports. 2020; 7(2): 112-116
5. Wang C, Baranchuk A. Long-term evolution of patients treated for early disseminated Lyme carditis. Third prize at the ICE 2021 (International Congress on Electrocardiology)
6. Besant G, Wan D, Yeung C, Blakely C, Branscombe P, Suarez-Fuster L, Redfearn D, Simpson C, Abdollah H, Glover B, Baranchuk A. Suspicious Index in Lyme Carditis (SILC): Systematic Review and Proposed New Risk Score. Clin Cardiol 2018; 41(12):1611-1616


For more:

Vector Biology: Connecting Human Health, Animal Health & the Environment

Vector Biology: Connecting human health, animal

health and the environment

Mount Allison University

Lyme Research Network

Vett Lloyd, Chris Zinck, Samantha Bishop

Vector-Biology-Connecting-human-health-animal-health-and-the-environment-Vett-Lloyd(1)   Slides Here 


Important Findings:

Donor 1
Borrelia was detected by nPCR, FISH and protein was detected by immunohistology in biopsied thoracic artery tissue. It was not detected in the other cardiac tissues.
▪ Borrelia burgdorferi DNA present only at low abundance in connective tissue
▪ These results validate the clinical diagnosis of Lyme disease in this individual, US serology and tick exposure
▪ Limited detection is consistent with aggressive treatment, although Borrelia DNA was detected. Viability cannot be assessed by these methods.
Round body more common than long/spriocheatal forms
▪ The individual is still well, active and healthy

Donor 2
▪ Abundant Borrelia was detected by FISH in the pericardium
▪ Other tissues still to be tested
▪ These results are consistent with tick exposure and US WB but not Canadian serology
Round body more common than long/spriocheatal forms
▪ Involvement of Borrelia infection in donor 2’s heart failure is an important question for the family and for all individuals living in endemic areas


➢ This study demonstrates that Borrelia DNA can be detected in human tissues using molecular methods