Coronary artery spasm

[dreamwheel]

I have a history of mi with sudden cardiac arrest. Can my spasms make me have another heart attack with sudden cardiac arrest? I am really tired of the chest pain. I take Imdur, Ranexa, and sublingual nitroglycerin. Is there anything else that I can do for these spasms?

[kenkeith]

Correction:   It is true using your analogy that a electrical pump will increase volume and will cause pressure to rise within the segment that has resistence....but the point is that on the other side of the resisted area, it does NOT have an increase in volume (CO output if you will).  

[kenkeith]

you assumed wrong, I defined CO on the thread...look up the meaning for yourself!.  It is beat stroke times heart rate for 1 minute.  Reread and you may understand.  If you didn't factor in CO's true meaning you will be confused, and you assumed it was carbon dioxide that will further confuse.  By the way to correct your misunderstanding further, CO is carbon monoxide and carbon dioxide is C02 :)

QUOTE: "When all arteries are fully forced open, an increase in heart rate will definitely increase blood pressure".

>>>>>A RELAXED vessel with medication will provide LESS RESISTANCE and will easily dilate due to less resistance.  It seems you are putting the cart before the horse as it were.  
As the name implies, vasodilator drugs RELAX the smooth muscle in blood vessels, which causes the vessels to dilate, and with all other factors remaining equal.  The equation is dilation of arterial (resistance) vessels leads to a reduction in systemic vascular resistance, which leads to a fall in arterial blood pressure. Dilation of venous (capacitance ) vessels decreases venous blood pressure.

Your fomula and lack thereof appears to be forced dilatation (rather than relax vessels) and an increased heart rate (not necessarily true that CO is increased):  One also should consider the total surface area of the vessel the blood is moving through as a factor: the larger the surface area, the slower the blood will move (velocity). Resistance to blood flow, such as that caused by a closed valve, is another thing which can influence the rate at which blood flows through the body.  

Organic nitrates have a direct relaxant effect on vascular smooth muscles, and the dilation of coronary vessels improves oxygen supply to the myocardium.  It is true using your analogy that a electrical pump will increase volume and will cause pressure to rise within the segment that has resistence.,,,but the point is that on the other side of the resisted area does have an increase in volume (CO output if you will). There is no medical finding I know about that relaxed vessels have a negative effect on the cardiovascular physiology?  Doesn't make sense. If the heart requires more blood/oxygen, system vessels constrict to help provide more blood/oxygen to vital organs.  If the vessels don't restrict, there could be cardiac arrest.

QUOTE: "If my heart didn't increase its rate, I'm sure I would have blacked out".

>>>You may be referring hypovolemic shock.  Meaning a substantial decrease in cardiac output (CO) such as heart failure, arrhythmia, loss of blood, etc. will drop blood pressure to a dangerously low level. Emergency treatment would be to increase CO (transfusion), respiration, etc. and if successful that may help stablize blood pressure.  

Thanks for your question,

[ed34]

We are talking about forcing the arteries fully open here, and not how the body 'normally' would function. It is not normal for every artery in the body to suddenly fully dilate and has nothing to do with gases or beds. I presume you mean CO2 by the way? not carbon oxide?
When all arteries are fully forced open, an increase in heart rate will definitely increase blood pressure. It isn't a misconception, it's a fact. Any electrical pump is the same, turn up the speed and hey presto, more pressure. I think you are overlooking the simple fact that the nitrates are forcing the vessels open, they cannot constrict to compensate for anything. If my heart didn't increase its rate, I'm sure I would have blacked out.

[kenkeith]

ED34 QUOTE: "They explained that the sudden drop in pressure due to the good elasticity of my vessels, causes my heart to work much harder, causing angina to worsen...Does the heart play a part in blood pressure? of course it does. Stop your heart, pressure drops and you die...

>>>>>That's funny, I can't believe you are serious, but for the reader that may have some interest in the etiology of systemic hypertension, the mechanism to lower blood pressure with medication is to dilate vessels and that doesn't cause the heart to "WORK MUCH HARDER"  Just the opposite; ACE inhibitor medication when effective increases the diameter of the vessel (dilate) decreases blood pressure (less resistance) and the burden for the heart is less...it doesn't worker harder!! =)

SOURCE: "ACE inhibitors block the conversion of angiotensin I to angiotensin II.  They therefore lower arteriolar resistance and increase venous capacity; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance."

QUOTE: Q: "My heart worked harder trying to raise blood pressure, while suffering even more through low oxygen. CCB definitely helped a lot more."

>>>> Do you mean the heart worked harder to perfuse more oxygenated blood to ischemic areas of the heart? Low oxygen...do you mean hypoxia of heart tissues?  CCB may be helpful under those circumstances?!  When the cardiac output (amt. of blood pumped in a minute!) is low, this alerts the kidneys to produce more volume. The increased unnecessary volume adds stress to the heart so I diuretic may be prescribed asd well as raising the cardiac output..

There appears to be some confusion or something misread  very old 75 has misled you. The heart doesn't work harder to raise blood pressure...the heart works harder to OVERCOME the high resistance of vessel constriction.  That is a very basic conception, but sometimes one may be confused.

Source: "The vascular beds are a dynamic and connected part of the circulatory system against which the heart must pump to transport the blood. Cardiac output is influenced by the resistance of the vascular bed against which the heart is pumping. For the right heart this is the pulmonary vascular bed, creating Pulmonary Vascular Resistance (PVR), while for the systemic circulation this is the systemic vascular bed, creating Systemic Vascular Resistance (SVR). The vessels actively change diameter under the influence of physiology or therapy, vasoconstrictors decrease vessel diameter and increase resistance, while vasodilators increase vessel diameter and decrease resistance. Put simply, increasing resistance decreases CO; conversely, decreased resistance increases CO".

___________
Although CCB may be helpful for certain conditions, it may be contraindicated for those who have had a heart attack and weaker than normal contractions. A good doctor would be aware.

[joanincarolina]

I have almost daily vasospasms of the microvessels of the heart. As the previous posters stated, a CCB may be very helpful in settling down the irritability of the heart's vessels and slow down those spasms. The cardiac pain may be coming from the smaller, unseen tiny vessels of your heart or it may be coming from the larger coronaries.Those spasms can cause temporary loss of blood flow to the heart muscle causing pain, but not necessarily damage. I've had these spasms for years and a recent functional MRI of the heart showed no heart wall problems. Discuss this CCB with your doctor. Imdur and Ranexa should assist you also. Keep the nitro handy and use it if you need it; don't second guess chest pain. Joan.

[ed34]

There are three basic parameters involved in blood pressure control in the body. I'm ignoring gravity and vein valves. The basic ones are heart rate/volume, artery constriction/dilation and of course blood volume. Does the heart play a part in blood pressure? of course it does. Stop your heart, pressure drops and you die. The heart gives out an average volume with each stroke, e.g mine is around 70% and so if arteries increase the lumen size, then pressure will suddenly drop. If this happens with nitrates, you cannot alter pressure by constricting the arteries, so the heart has to compensate. Example, before nitrates, my heart rate was 68, as soon as I took nitrates it increased to 100-120.
So, what I am saying is, if angina is not evident at rest, but appears on exertion, then this will bring it on. When my heart rate was anything above 90, angina kicked in.
No I am not saying CCB is useful under those conditions, I'm saying personally I think it's a better control for spasms because it doesn't shock the arteries from one state into another, it slows their reaction down and makes it much harder for them to spasm. CCB are now commonly prescribed for spasms.
With regards to stiffer arteries. If you imagine a patient with stiff aged arteries, then a higher dosage of nitrates can be tolerated, enough to force open the diseased coronary arteries. Imagine a patient with very elastic arteries but diseased coronary arteries. Nitrates on a very low dosage will be enough to dilate the normal vessels, but will be too low a dosage to open the diseased ones. A dosage high enough to open diseased vessels causes too much of a pressure drop in the body for those patients, hence the side effects of chronic headaches. I remember in hospital this was explained to me because a 75 year old man in the next bed had the same dosage as me, and he was acting like nothing had happened. I went as white as a sheet, felt dizzy/nauseous and the headaches were like I had never felt before. Have you heard of Nicorandil? it's given to old people in 10mg. I was given 5mg and I couldn't stand up. The ward was spinning too fast.
I have a feeling that the medications in use are standardised after many years of usage, but heart disease was always known as an old persons disease. Now it appears younger people are being affected with the disease and the medications are causing effects not expected. I know a man of 38 who has heart disease and he can't tolerate any medication at all, not even beta blockers.

[kenkeith]

My health history has alway been proper weight, almost normal blood pressure (slightly high systole (if I had "stiff" arteries, it would show a high systole abnormally), cholesterol below 149, etc.  Don't judge by age!  My parents had a long healthy life without ever being on any medication until the final days..

I took good health for granted at a very young age.  Smoked, binge drinking. improper diet, all night parties, etc. I was shocked to learn I had had a silent heart attack 6 years ago, but I had worked on a project for a couple of days without a mask in dusty, and chemically polluted enclosed area. I always felt good, and I still do...but medication does have some side effects...less energy and I believe that is due to statins (I'm not sure benefits out weigh risks).  I'm looking at my emergency report and it says Chol 132, HDL 49, LDL of 71. Tropnin level 0.40.  Patient's ejection fraction was found to be 29%.   Cath stated13% go figure!

QUOTE: "They explained that the sudden drop in pressure due to the good elasticity of my vessels, causes my heart to work much harder, causing angina to worsen."

>>>>I'm not sure I understand.  Dilated vessels (better elasticity) shouldn't cause heart to work harder.  Increase the diameter of the vessel (dilate) decreases blood pressure (less resistance) and the burden for the heart is less...it shouldn't work harder.  

Also, IF may vessels are stiffer than yours, then it would seem, following what you have said, nitrates would not be effective for me.  I'm not sure of cell and muscle biology, but it sounds plausible that stiff vessels may not dilate adequately with nitrate and be ineffective.

Q: "My heart worked harder trying to raise blood pressure, while suffering even more through low oxygen. CCB definitely helped a lot more."

>>>>I don't quite understand!  Do you mean the heart worked harder to perfuse more oxygenated blood to ischemic areas of the heart? Low oxygen...do you mean hypoxia of heart tissues?  CCB may be helpful under those circumstances?!

[ed34]

You have to remember you are a fair bit older than I Kenkeith, so your arteries will most likely be much stiffer than mine, or the posters, and this makes nitrates feel more nasty to us. Having had several scans of arteries around my body, the only ones which seem affected are the coronary and cardiologists have said this is probably why nitrates make me feel particularly bad. They explained that the sudden drop in pressure due to the good elasticity of my vessels, causes my heart to work much harder, causing angina to worsen. Not the effect I am looking for. The dosage given was enough to open healthy vessels, but not enough to open stiff plaqued vessels, so not helping at all.
With regards to CCB, there are different agents of this medication. At one end of the scale there are CCB which are ideal and often used to treat angina. While at the other end of the spectrum there are agents used to relax the stiff arteries of the elderly. I suffered vasospasm for a few months, kicked off by angioplasty, but nitrates just made it worse. My heart worked harder trying to raise blood pressure, while suffering even more through low oxygen. CCB definitely helped a lot more.

[kenkeith]

Sublingual nitroglycerin is a fast acting (within minutes) to relieve angina (chest pain due to lack of blood/oxygen to heart cells).  I take a nitrate and that stays effective for the day.  As stated one can develop a tolerance but with a brief intermissions that problem does not exist, and the underlying cause properly treated should be the course of action.  

Heart related spasms indicate the heart is not getting enough blood oxygen, and as a result there can be heart cell damage and over a period of time untreated may cause heart wall movement impairment with stunned or necrotic heart cells.

Wikipedia: "Calcium channel blockers frequently are used to control heart rate, vasospasm, and reduce chest pain due to angina pectoris. Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy" . If you prior MI has reduced your heart's ability to pump effectively (low EF) CCB may be contraindicated for your medical condition.  Discuss with your doctor, and maybe switching to a nitrate with an increase or adjusted dose (has less acting chemical agent than nitro) will help.  Take care.

[ChatterAlly]

I take Norvasc for the spasms.  Have you talked to your doctor about being put on a calcium channel blocker?  It took a couple of weeks to start feeling the full effects of this drug, but my spasms have been quieted down for a few months now.  Like you, I thought for sure that I was going to have a heart attack.  It takes some work to find the right medication some times. Nitrates are a great way to relief the symptoms, but you need a medication that will treat the problem.  Take care, Ally

[ed34]

Hi, you say you have a history, but there's something a bit unclear. Your medication. Do you still have sudden MI with the medication you are on now, or has the current medication regime so far stopped them? you say you still get chest pains.
Your medication is highly based on nitrates which are a way to try and force the arteries open all the time. Your body can get used to these and the effects can lessen over time, but perhaps you could ask your Doctor to try a different approach. Rather than trying to force the arteries open all the time with nitrates (which isn't always successful with spasms), you could try Calcium channel blockers. Arteries have a smooth muscle in the walls which are used to constrict or relax the vessels, and to do this they require Calcium from the blood travelling through them. The Calcium is extracted from the blood through tiny channels in the artery lining and the less Calcium the muscle can get, the harder it is for them to do any work. Calcium channel blockers restrict the Calcium intake to the artery muscle and in theory this should disable its ability to go into a violent spasm because it has a limited amount of calcium to do the work. Calcium channel blockers are quite successful in many people but they also have an added bonus. As Calcium channel blockers only work on smooth muscle type, they also affect the heart because this too is smooth. The CCB act as a kind of beta blocker, keeping the heart from over working.
So rather than trying to keep your arteries forced open, which would be difficult against a spasm, you would be restricting a chemical needed for spasms, making it so the arteries can only react to body changes more slowly. I was on these for a month and felt no strange effects, but I certainly did with nitrates, I hated them. I continually had headaches and felt dizzy with them.