Without durable individual immunity you cannot even talk about herd immunity

 In the early days of the covid 19 pandemic there was much speculation about what percent of the population would have to be vaccinated in order to achieve herd immunity )(HI). It seemed to be a matter of not if but when HI would be accomplished.

Writers made analogies to  measles and smallpox for which vaccination programs achieved herd immunity and in the case of smallpox, eradication. If HI could be achieved  for a  very infectious disease such as measles spread by aerosols, why not covid 19?

Theoretical considerations regarding HI center on the basic reproduction number (R naught or Ro which is the average number of people that one infected person will infect.  The number of people needed to be immunized in order to reach HI is 1-1/Ro.For example-if the Ro is 2 then 50% would have to become immune (either through vaccination or infection) for a Ro 0f 3 we see 1-1/3 equals 2 thirds or 67% 

Several simplifying assumptions underlie the formula for HI including that all individuals have an equal opportunity to become infected. Epidemiologists disagree as to what exactly HI is and as to what the necessary assumptions are in estimating a HI vaccination level.

However the key-typically implicit- assumption is that being vaccinated ( or recovering from an infection) results in long lasting immunity.(1)

We now know that this major assumption does  not conform with reality. We now know that fully immunized individuals can become infected and can transmit the disease and also  that recovery from covid 19 infection does not preclude becoming infected again. 

The idea underlying HI is that as individuals become vaccinated ( or recover from infection) they are removed from the susceptible pool. With covid vaccination or infection  both groups seem to be removed from that pool only for a time , perhaps as short a time as 6-8 months. While infection blocking immunity (nasal mucosal immunity) wanes quickly the disease reducing immunity seems to be more durable.

When cases of abreakthrough infection became recognized as a real thing,some in the public health sector  said  " well, the vaccine was only intended to prevent serious disease and death".But if that were the case why was there so much  talk about achieving herd immunity a concept that IMO only makes sense if the vaccine prevents spread.

Dr Jennie S Levine has been quoted that she and her colleagues talk about transient herd immunity.

My thought on that is perhaps we are seeing a transient HI for example now In Louisiana and Texas .Both states had a major Delta surge with a surge of cases and hospitalization and death and now the surge seems to have abated.Possibly as more and more people were vaccinated and more infection plus mandatory NPIs (in Louisiana ) the number of susceptible individual decreases to reach some level of transient herd immunity like condition. However, as immunity wanes again in states with a large number of unvaccinated individuals serving as a covid reservoir some level of spread could occur again  for another round of surges . Are we likely to continue to see regional whack a mole events .

A much more optimistic scenario is that the booster shots will bring about a sufficiently long period of immunity so that more than a transient herd immunity could be achieved. In other words- the covid 19 mRNA vaccine should have been a three shot vaccination  program all along.  

1)Core Concept: Herd immunity is an important—and often misunderstood—public health phenomenon | PNAS

How big will the US covid winter surge be?

The epidemiology  predictors at IMHE made their prediction for the 2021 winter on a tweet published November 5.

Based on three factors they predicted there will be a winter surge but, of course its magnitude is unknown.

The factors are : 1) seasonality 2) waning vaccination immunity 3)less caution by the public,We think we know the direction of these vectors but what about their magnitudes?

As time goes on not only vaccine immunity will fade but so will the immunity of previous covid 19 infection  both of which seem to fade in about six months.   Countering that direction is the number of people receiving the booster shots.Countering that is the relentless barage from right wing media claiming that the vaccines are either dangerous or worthless.

Meanwhile in France and Germany a new surge seems underway and travel restrictions to to the US have been lifted. What could possibly go wrong?

Dr. Michael Osterholm is quoted: "Any effort to predict future course beyond 30 days relies on pixie dust for its basis" and we all remember what Yogi said about predictions particularly for the future.

Cardiac fibrosis in endurance athletes

 There have been a number of reports of cardiac fibrosis in endurance athletes. It turns out that these reports pertain to areas of late gadolinium enhancement in right ventricular insertion points.Some explanation is required . To begin with-all forms of fibrosis are not the same.

Gadolinium is the contrast agent  used in MRIs.It accumulates in the extracellular space and lights up on a cardiac MR and is called Late Gadolinium Enhancement (LGE)

LGE is seen in myocardial infarctions in necrotic areas with scars consisting of replacement fibrosis.LGE has also been reported in hypertrophic cardiomyopathy (HCM) ,pulmonary hypertension and more recently in a number of long time highly trained endurance athletes.In these three conditions the underlying pathology is not replacement fibrosis  (as is seen in a myocardial infarction scar) but rather plexiform fibrosis and myocardial fiber disarray and is typically seen at the insertion points or hinge points where the right ventricular wall inserts on the interventricular septum. 

Sato et al (1) proposed  that paradoxical motion of the interventricular septum is a primary mechanism for late gadolinium enhancement (LGE) at the ventricular insertion or hinge points.

LGE at ventricular insertion points has been described in pulmonary hypertension and in a number of highly trained endurance athletes .It is unlikely that paradoxical septal movement explains the LGE at hinge points in these athletes although it may be  true in the cases described by Sato.

DeBosscher et al (2) found LGE at the hinge points in young and older highly trained endurance athletes but found no evidence that LGE was associated with any structural,functional or electrical problem with LGE at the insertion points which they found  28% of the 233 athletes studied.

LGE was first described in  older endurance athletes   but now this data demonstrates that younger runners may also have that finding and that it is not a uncommon findings in highly trained runners and its long term significance remains to be determined. I suppose the fact that the LGE does not represent replacement fibrosis  with its associated risk of reentrant ventricular tachycardia  is good news.However,data is lacking as to the long term consequences (if ANY) of LGE at the RV insertion points in long time endurance athletes regarding reentrant rhythms or other clinical problems. 

1) Sato,t et al Paradoxical motion of the interventricuar septum as a primary mechanism of ate gadolinium enhancement at ventricular insertion points. Int J Cariol 2012;158 (1) 156-7 

2)De Bosscher, R et al Hinge point fibrosis in athletes is not associated with structural, functional or electrical consequences;a comparison between young and middle aged elite endurance athletes. Euro Heart Journal, 41,supp 2, Nov 2020 

What is the threshold for exercise induced cardiac remodeling (EICR)

 It has been known for over 100 years that physical exercise  may cause heart enlargement.A study of Harvard rowing team members described cardiac enlargement in an 1899 issue of the Boston Medical Surgical Journal.  

There have been numerous cross sectional and longitudinal studies documenting the structural changes in the heart associated with high levels of aerobic exercise.These  are enlargement of all four chambers and mild to moderate increase in the left ventricular wall thickness and an increase in left ventricular mass index- a condition referred to as eccentric hypertrophy to be distinguished from the concentric hypertrophy characteristic of strength building exercise. 

How much exercise is required to bring about that remodeling? Is  eccentric remodeling observed in runners whose activity  level is far less that that required  to be competitive in a full triathlon ?

Dawes and associates  (1) have provided some answers.They performed cardiac mri s on 1096 volunteers and linked  the mr results with their self reported exercise habits over the previous 12 months. They divided the exercise histories into four categories with category 1 being essentially no regular aerobic exercise and category 11 defined as less than or equal to 3 hours per week. They found that there was no statistical difference between category I and category 11 in regard to cardiac MR findings/

So one 'take- home" from their study might be  that exercise less than 3 hours per week is not likely to be associated with any exercise related structural cardiac changes. 

Moreover they found that increasing activity levels were significantly associated with increased ventricular end-diastolic volumes and left ventricular mass index

However, minutes exercised is not the only variable related to EICR which is likely related to some summation or interaction between intensity, frequency and duration. One could speculate that someone doing 3 hours of high intensity interval training per week  might well induce a bit of EICR and that someone doing 8 hours of slow walking in the park per week may probably would not

1) Dawes TJW Moderate physical activity in healthy adults is associated with cardiac remodeling.Circ Cardiovascular imaging 2016  se004712