Is this an alarm that we should swim more to strengthen our hearts? Though similar tragedies happened to swimmers in the past, too, I believe. Seems all are in their late 50's?
News from
www.newsday.com/.../ny-nyrun0312133574nov03,0,6679842.story
Marathon runner dies after collapsing at finish line
BY DANIEL EDWARD ROSEN9:32 PM EST, November 2, 2008
A 58-year-old runner who had just finished the New York Marathon Sunday collapsed at the finish line after going into cardiac arrest and later died at a local hospital, police said.
Carlos Jose Gomes, of Sao Paolo, Brazil, was pronounced dead at Lenox Hill Hospital at about 5:20 p.m., police said. He had fallen ill after he crossed the finish line of the 26.2 mile race near the intersection of 81st Street and Central Park West.
Two other people suffered cardiac arrest Sunday while running in the race, police said.
A 59-year-old man collapsed in the middle of the Queensboro Bridge, police said. A fellow runner stopped and administered CPR until two emergency medical technicians arrived.
The runner was taken to New York-Presbyterian/Weill Cornell Medical Center, where he was listed as critical but stable, according to one of the EMTs.
Jean-Louis Maubaret, 59, a French national, was running alongside his wife across the Queensboro Bridge between the 15th and 16th mile of the race when he collapsed, unconscious and not breathing, according to EMT Salvatore Sangeniti.
Sangeniti, 47, of the New York Fire Department EMS Division 4, was crossing the bridge from the Manhattan side when he and his partner, Amanda Wong, received a radio call about the runner. They reached the middle of the bridge to find another runner performing CPR.
Sangeniti, of Centereach, said he placed a defibrillator on Maubaret's chest. After one shock, he said, the runner regained consciousness and resumed breathing.
The runner who performed CPR returned to the race once he saw that Maubaret had regained consciousness, Sangeniti said.
Another marathoner suffered cardiac arrest on East 107th Street yesterday afternoon. The man, whose name was not immediately known, had collapsed and was not breathing, according to an FDNY spokesman. EMTs performed CPR as he was rushed by ambulance to Mount Sinai Medical Center.
"The majority of sudden deaths occurring in middle aged athletes are due to atherosclerosis with plaque rupture resulting in myocardial infarction (heart attack) and ventricular fibrillation."
So you are saying that the plaque rupture blocks one of the coronary arteries, the resulting blood insufficiency to heart muscle triggers the ventricular fibrillation, the ventricle then ceases to pump effectively, and the victim dies from systemic oxygen/nutrients depletion rather than merely just heart muscle insufficiency?
In other words, the m.i. triggers the v-fib?
If the m.i. does not trigger v-fib, and does not block so much blood flow to the heart that parts of it can continue to function a little, then the so-called coronary thrombosis patient (again, the "classic" heart attack) has pain and other symptoms, but can last for hours or longer, correct? It's only when v-fib (or other catastophic arrythmias) is triggered that he or she has only minutes to live, right?
Isn't it also possible that electrolyte imbalances, heat stress, pre-existing vulnerabilities in the heart's electrical system, etc. are also causes for v-fib in highly exertional exercise? When they do autopsies of victims of sudden cardiac death in exercisers, do most of the victims have evidence of blocked arteries that acted as the first domino and triggered the v-fib?
Let me paste in an excerpt from a story I wrote on this recently:
Another external culprit: extreme disturbances in the salts the body uses to propagate electrical signals. Ironically, this can happen in guys who otherwise epitomize robust health. So-called hyponatremia of exercise, for instance, strikes when endurance athletes drink too much water to remain well-hydrated in the heat while failing to replace the sodium and other key electrolytes they're sweating away. Despite revised fluid replacement guidelines from organizations like USA Track and Field,some runners continue to over-hydrate themselves literally to death.
"The electrical system of the heart relies on sodium and potassium and calcium to work," says William H. Maisel, MD, MPH, director of the Pacemaker and Device Service at Beth Israel Deaconess Medical Center. "If these get too far out of whack, it can lead to cardiac arrest--something that unfortunately still happens at almost every major marathon."
By far the most common cause of arrhythmias, however, are changes to the heart caused by the aging process itself, especially when this includes all-too-common co-travelers like high blood pressure, valve damage, and other forms of heart disease. It turns out, for instance, that cells in the sinus "pacemaker" are not the only ones capable of firing off an inaugurating electrical signal. Every cardiac muscle cell has this ability--and with age, the tendency increases for "loose cannons" to fire spontaneously, usurping the sinus's role
*
Billy, as far as ibuprofen goes, as common as it is to pop a bunch of these and then go exercise, it's not a good idea. Besides kibboshing the prostaglandins that foster inflammaton, NSAIDs also hamper the prostaglandins that protect the stomach lining (causing ulcers or low grade bleeding in some people) and, even more importantly, hinder the prostaglandins that promote fluid flow through the kidneys. If you become dehydrated, and take a lot of NSAIDs, you are at risk for kidney failure. Though not common, one fellow after the Boston Marathon did precisely this and went into kidney failure on his flight home.
The evidence that NSAIDs promote healing is sketchy at best; most so-called tendinitis conditions are, in fact, tendonopathies--you want to foster blood flow to poorly vascularized tissues (like the Achilles tendon, knee, tennis elbow, shoulder, plantar fascia) rather than inhibit inflamation here. Hence newer techniques like nitroglycerine patches for some of the slow healing areas.
Just my layman's point of view based on hearing a talk about this at the ACSM conference and readings hither and yon from medline.
"The majority of sudden deaths occurring in middle aged athletes are due to atherosclerosis with plaque rupture resulting in myocardial infarction (heart attack) and ventricular fibrillation."
So you are saying that the plaque rupture blocks one of the coronary arteries, the resulting blood insufficiency to heart muscle triggers the ventricular fibrillation, the ventricle then ceases to pump effectively, and the victim dies from systemic oxygen/nutrients depletion rather than merely just heart muscle insufficiency?
In other words, the m.i. triggers the v-fib?
If the m.i. does not trigger v-fib, and does not block so much blood flow to the heart that parts of it can continue to function a little, then the so-called coronary thrombosis patient (again, the "classic" heart attack) has pain and other symptoms, but can last for hours or longer, correct? It's only when v-fib (or other catastophic arrythmias) is triggered that he or she has only minutes to live, right?
Isn't it also possible that electrolyte imbalances, heat stress, pre-existing vulnerabilities in the heart's electrical system, etc. are also causes for v-fib in highly exertional exercise? When they do autopsies of victims of sudden cardiac death in exercisers, do most of the victims have evidence of blocked arteries that acted as the first domino and triggered the v-fib?
Let me paste in an excerpt from a story I wrote on this recently:
Another external culprit: extreme disturbances in the salts the body uses to propagate electrical signals. Ironically, this can happen in guys who otherwise epitomize robust health. So-called hyponatremia of exercise, for instance, strikes when endurance athletes drink too much water to remain well-hydrated in the heat while failing to replace the sodium and other key electrolytes they're sweating away. Despite revised fluid replacement guidelines from organizations like USA Track and Field,some runners continue to over-hydrate themselves literally to death.
"The electrical system of the heart relies on sodium and potassium and calcium to work," says William H. Maisel, MD, MPH, director of the Pacemaker and Device Service at Beth Israel Deaconess Medical Center. "If these get too far out of whack, it can lead to cardiac arrest--something that unfortunately still happens at almost every major marathon."
By far the most common cause of arrhythmias, however, are changes to the heart caused by the aging process itself, especially when this includes all-too-common co-travelers like high blood pressure, valve damage, and other forms of heart disease. It turns out, for instance, that cells in the sinus "pacemaker" are not the only ones capable of firing off an inaugurating electrical signal. Every cardiac muscle cell has this ability--and with age, the tendency increases for "loose cannons" to fire spontaneously, usurping the sinus's role
*
Billy, as far as ibuprofen goes, as common as it is to pop a bunch of these and then go exercise, it's not a good idea. Besides kibboshing the prostaglandins that foster inflammaton, NSAIDs also hamper the prostaglandins that protect the stomach lining (causing ulcers or low grade bleeding in some people) and, even more importantly, hinder the prostaglandins that promote fluid flow through the kidneys. If you become dehydrated, and take a lot of NSAIDs, you are at risk for kidney failure. Though not common, one fellow after the Boston Marathon did precisely this and went into kidney failure on his flight home.
The evidence that NSAIDs promote healing is sketchy at best; most so-called tendinitis conditions are, in fact, tendonopathies--you want to foster blood flow to poorly vascularized tissues (like the Achilles tendon, knee, tennis elbow, shoulder, plantar fascia) rather than inhibit inflamation here. Hence newer techniques like nitroglycerine patches for some of the slow healing areas.
Just my layman's point of view based on hearing a talk about this at the ACSM conference and readings hither and yon from medline.
