I’ve been grieving the loss of my fiancé for the last nine months. The last three nights in a row, chest pains that feel like my heart have awakened me. At random times I feel her calling me to join her on the other side.
“In time, Love, in time,” I say.
I still have things I want to do here.
Broken heart syndrome, according to Dr. Macola, gives you a much greater risk of heart attack.
Broken heart syndrome (stress cardiomyopathy or takotsubo cardiomyopathy) is a real medical condition, triggered by acute, major stress or shock, such as the death of a loved one.
Studies have shown that the loss of a loved one raises your own risk of sudden death, known as the “bereavement effect.” There’s even evidence showing that spousal illness increases the partner’s mortality risk
I’ve had four of the most stressful events a person can experience within the last nine months: trumatic death, loss of primary relationship, change of career, and moving.
Even before these stressors I had occasional bad heart pains and arrhythmia. When I passed my treadmill tests, chest x-rays showing either fluid or scar tissue at the base of both of my lungs. I did go to the ER once with pleurisy, pain from the lung lining sticking to the chest wall due to inflammation, so what I’m experiencing now could be that again, inflammation.
What can I do to avoid the Grim Reaper a while longer?
The real revolution in the prevention and treatment of heart disease will come with increased understanding of the role played by the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart rate variability (HRV). We have two distinct nervous systems: the first, the central nervous system (CNS), controls conscious functions such as muscle and nerve function; the second nervous system, the autonomic (or unconscious) nervous system (ANS), controls the function of our internal organs.
The autonomic nervous system is divided into two branches, which in a healthy person are always in a balanced yet ready state. The sympathetic or “fight-or-flight” system is centered in our adrenal medulla; it uses the chemical adrenaline as its chemical transmission device and tells our bodies there is danger afoot; time to activate and run. It does so by activating a series of biochemical responses, the centerpiece of which are the glycolytic pathways, which accelerate the breakdown of glucose to be used as quick energy as we make our escape from the bear chasing us.
In contrast, the parasympathetic branch, centered in the adrenal cortex, uses the neurotransmitters acetylcholine (ACh), nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) as its chemical mediators; this is the “rest-and-digest” arm of the autonomic nervous system. The particular nerve of the parasympathetic chain that supplies the heart with nervous activity is called the vagus nerve; it slows and relaxes the heart, whereas the sympathetic branches accelerate and constrict the heart. I believe it can be shown that an imbalance in these two branches is responsible for the vast majority of heart disease.
Using the techniques of heart rate variability (HRV) monitoring, which gives a real time accurate depiction of autonomic nervous system status, researchers have shown in multiple studies that patients with ischemic heart disease have on average a reduction of parasympathetic activity of over one-third. Typically, the worse the ischemia, the lower the parasympathetic activity.
Furthermore about 80 percent of ischemic events are preceded by a significant, often drastic, reduction in parasympathetic activity.
By contrast, those with normal parasympathetic activity, who experience an abrupt increase in sympathetic activity (such as physical activity or an emotional shock), never suffer from ischemia.
In other words, without a preceding decrease in parasympathetic activity, activation of the sympathetic nervous system does not lead to MI.
Presumably we are meant to experience times of excess sympathetic activity; this is normal life, with its challenges and disappointments. These shocks only become dangerous to our health in the face of an ongoing, persistent decrease in our parasympathetic, or life-restoring, activity.
The decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: acetylcholine, NO, and cGMP. It is fascinating to note that women have stronger vagal activity than men, probably accounting for the sex difference in the incidence of MI.
Hypertension causes a decrease in vagal activity, smoking causes a decrease in vagal activity, diabetes causes a decrease in vagal activity, and physical and emotional stress cause a decrease in parasympathetic activity.
Thus, all the significant risk factors suppress the regenerative nervous system activity in our heart. On the other hand, the main drugs used in cardiology upregulate the parasympathetic nervous system.
Nitrates stimulate NO production while aspirin and statin drugs also stimulate the production of ACh along with NO—that is, until they cause a rebound decrease in these substances which then makes the parasympathetic activity even worse. Beta-blockers work by blocking the activity of the sympathetic nervous system, the increase of which is a central factor in the etiology of MI. The bottom line: the risk factors for heart disease and the interventions used all affect the balance in our ANS; whatever effects they may have on plaque and stenosis is of minor relevance.
… First comes a decrease in the tonic, healing activity of the parasympathetic nervous system—in the vast majority of cases the pathology for heart attack will not proceed unless this condition is met. Think of the person who is always pushing himself, who never takes time out, who has no hobbies, who constantly stimulates the adrenal cortex with caffeine or sugar, who does not nourish himself with real food and good fats, and who does not incorporate a regular pattern of eating and sleeping into his daily life.
Then comes an increase in the sympathetic nervous system activity, usually a physical or emotional stressor. This increase in sympathetic activity cannot be balanced because of chronic parasympathetic suppression. The result is an uncontrolled increase of adrenaline, which directs the myocardial cells to break down glucose using aerobic glycolysis. Remember that in a heart attack, there is no change in blood flow as measured by the p02 in the cells. This step shunts the metabolism of the heart away from its preferred and most efficient fuel sources, which are ketones and fatty acids.
This explains why heart patients often feel tired before their events. This also explains why a diet liberal in fat and low in sugar is crucial for heart health. As a result of the sympathetic increase and resulting glycolysis, a dramatic increase in lactic acid production occurs in the myocardial cells; this happens in virtually one hundred percent of heart attacks, with no coronary artery mechanism required. As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis prevents calcium from entering the cells,16 making the cells less able to contract.
This inability to contract causes localized edema (swelling), dysfunction of the walls of the heart (hypokinesis, which is the hallmark of ischemic disease as seen on stress echoes and nuclear thallium stress tests), and eventually necrosis of the tissue—in other words, a heart attack. The localized tissue edema also alters the hemo-dynamics of the arteries embedded in that section of the heart, resulting in shear pressure, which causes the unstable plaques to rupture, further block the artery, and worsen the hemodynamics in that area of the heart.
Please note that this explanation alone explains why plaques rupture, what their role in the heart attack process is, and why they should indeed be addressed. Notice also that this explanation accounts for all the observable phenomena associated with heart disease and is substantiated by years of research. It could not be clearer as to the true origin of this epidemic of heart disease. …
I do not discount the mental game. There is a debate about optimism versus pessimism, which I think boils down to resulting parasympathetic activity. In other words, being pessimistic can make some people relax because anything bad that happens is just what they expected. Optimism can make others relax because they don’t worry about bad things in the future. The important thing is to relax and rejuvenate.
The reason is, good microcirculation happens when you relax. Microcirculation is the movement of the blood in the smallest blood vessels present in the vasculature embedded within organ tissues, including heart tissue.
Here’s my current heart health protocol:
- Try to get 7 1/2 hours sleep per night.
- Meditate daily for 15 to 20 minutes.
- Take L-carnitine, co-Q10 and magnesium.
- Eat dark chocolate once in a while.
- Have a creative outlet.
- Get your heart rate up for at least a half hour to 45 minutes at least three times a week.
- Do some strength training every day has this keeps blood sugar regulated.
- Breathe only through your nose as this creates nitric oxide, a natural and powerful vasodilation gas.
- Spend time with people who relax you.
- Get a hug a day. Touch is a powerful healer.
- Stay active cleaning and organizing.
- Do yoga daily.
- Stay busy. Set up activities with friends.
- Try not to overwhelm yourself with grief.
There is research where new heart tissue has been generated in the lab. If we can hold out long enough, our odds may increase greatly with advances in medical science.