Keith Hickey, M.D.

A stress echocardiogram is just one type of stress test. Stress tests are done to evaluate coronary blood flow and muscle function. If a patient has significant atherosclerotic plaque in his coronary arteries (blocking more that 70% of the lumen), a stress test should be abnormal. Stress tests are screening tests designed for high sensitivity (no false negative tests) so a patient with coronary disease doesnt have a normal study. Specificity is less robust, with more false positive tests leading to some unnecessary coronary angiograms. Thats the downside. Each stress type has 2 basic components.. the stressor and the imaging modality used to evaluate the heart response to the stress. The 2 main stress types are exercise (treadmill) or vasodilator administration (regadenosine). The vasodilators mimic exercise for those patients that cannot walk on the treadmill or have certain underlying ECG abnormalities (paced rhythm or left bundle branch block) making the ECG uninterpretable. The imaging components can be treadmill ECG, treadmill echocardiogram or various nuclear imaging types that rely of sophisticated scintillator nuclear cameras. The nuclear images can be very high sensitivity and specificity up to PET-CT (>90%).. exercise is physiologic and preferably used over pharmacological agents (adenosine products). The regular treadmill uses a Bruce protocol, increasing speed and elevation every 3 minutes. Exercise times greater than 9 minutes are good. Greater than 12 are excellent. While exercising the ecg is continuously monitored for changes that indicate ischemia (blocked arteries) and arrhythmias. Also symptoms like chest pain or shortness of breath are noted. The test is done when target heart rate is reached. THR is 220-age x 0.85.. or 85% of maximum heart rate. The sensitivity of a regular treadmill stress test is

The general rule is one day to recover from an elective coronary stent, placed as an outpatient, for stable , chronic coronary disease. This assumes the procedure was performed without any complications, such as mechanical (coronary perforation, dissection ) related to stent deployment or downstream plaque dislodgment causing a peri-procedural myocardial infarction (heart attack). Normally outpatient PCI and stenting (percutaneous coronary interventional procedures with angioplasty balloons and stents) take an hour or less and the patient is stable for discharge home within 2 hours of radial artery access through the wrist. We keep them 4 hours if we access the femoral arteries in the groin. By the next day they are out and about. If complications develop they are kept in the hospital overnight to rule out extensive bleeding or MIs. Most would go home the next day. For very complicated PCIs, some patients are kept overnight as a precaution. With a severe tear in the artery resulting in life threatening, massive bleeding, then emergency coronary bypass grafting would have to be performed. This is quite rare (less than 1/2 to 1%) of outpatient elective procedures per year.these patients are more stable, generally healthier, and are coming from home to have the procedures done, for chronic, mostly stable disease. They either have stable,exertional, anginal chest pain, an abnormal stress test, or lastly, a staged intervention for a previously known blockage. By the next day, these patients are doing their usual activities. Those patients are different than the more critical patients admitted in the hospital for cardiac events (unstable angina or nonSTEMI). These patients present to the ER with signs and symptoms of a true heart attack or ACS ( acute coronary syndrome) . These patients have a ruptured atherosclerotic plaque that forms a clot inside the artery . This scenario becomes an urgent , if not emergent, medical situation. They are taken to the Cath lab that day or writhin 24 hours. There are protocols for each hospital with regards to the medications administered, the team called out from home, the nursing unit or ICU /CCU bed needed before and after the procedure. These patients generally stay in the hospital 1-2 days after the procedure, to ensure there are no post procedural complications such as arrhythmias, or extension of the MI, bleeding, etc. they have had a true cardiac event and will need 1-2 weeks to fully recover enough to go back to work and 4-6 weeks before strenuous activities can be resumed (once they are cleared by their cardiologist). Most of these do well, even when they push themselves to soon and regress for a few days. The recovery from the stent is still only a day or 2 but the recovery from the inciting event is days to weeks before they are 100%. The last case scenario is the true emergency, an STEMI. This type of heart attack is a true emergency and the artery is completely clotted off, with no blood flow to that part of the heart muscle. There will be extensive cardiac muscle loss and the complications from this range from electrical ( arrthymias , heart block) to mechanical ( perforations, aneurysms, valve rupture). These can cause cardiogenic shock or death within hours to days. When a patient comes to the ER with EMS, and their ECG shows an ST segment elevation) , we have one hour to get in and re-establish blood flow with clot removal (thrombectomy) angioplasty and stenting to the affected area. This is called the golden hour and it has been studied and proven clinically sacrosanct across many different studies and trials. This is a true medical emergency and if the muscle isnt saved the patients end up with cardiogenic shock and in-hospital mortality of 50%. They will never be the same if they do live. Time is muscle. Muscle death means patients death. The stent deployment and procedures are not much different , except that its done very fast. But the recovery is 1-2 days in the CCU and another 1-2 days in the step down unit. They are physically stressed and do little more than walk slowly in the hallways and to the bathroom. They will need 4-6 weeks at home before cleared to go to work. Many need 6 weeks of cardiac rehab. So the recovery from the stents might be a day or 2, but the recovery from this event in weeks to months .. of course it depends on the individual patient and the details of the hospital stay, procedure itself, any complications etc. some recover sooner than others. Most do recover if we are able to restore blood flow and oxygen to the tissue within the golden hour. (This is a very simplified explanation of these clinical scenarios and hours could be spent just explaining the different ST segment changes noted in the different kind of MIs). To close , the recovery frequency for most stents is a day or 2 and the recovery from open heart surgery or bypass surgery is 5-6 days in the hospital if all goes well. 2 weeks at home doing little but walking around the house .. after 6 weeks they can go to cardiac rehab and start walking regimen . Return to work is usually 4-6 weeks. In comparison, the return to work from an elective uncomplicated outpatient stent deployment is one day ..

Answer: I agree that your symptoms are atypical and not consistent with true anginal chest pain from coronary ischemia ( diminished tissue oxygenation from lack of blood flow due to obstructive atherosclerosis in the coronaries). Angina is usually suffocating, pressure

Answer: Your chest pain is not of primary cardiac nature. Any chest pain from ages 17-19 is secondary to another issue or process. The only myocardial abnormalities of any significance in your age group are congenital (you would have been born with the problem). But the symptoms are real. This is due to your underlying psychiatric issues, particularly the anxiety and panic attacks. You have years of significant mental health problems, including eating disorders. Bulimia-anorexia are ugly cousins and not to be taken lightly. In addition to that, you have untreated anxiety/depression/ panic attacks. You do need a psychiatrist and therapist in addition to a good support group at home. Mood altering chemicals like alcohol or MJ are not the answer. Im glad you stopped self medicating.. Now, what about the heart. Your pain is sharp and atypical and not due to any type of coronary disease. You have a problem with the autonomic nervous system as a result of your extreme anxiety and panic attacks. The symptoms are real but its your brain hijacking the cardiovascular system and your other organs. The most complex system in our body is the nervous system . We dont know more than we do know. The nervous system is under the control of the central nervous system , including the brain and spinal cord. Under the CNS umbrella you have a sensory nervous system (touch), motor nervous system to move our skeletal muscles. Smaller fibers of pain, temperature etc. our skeletal joints have proprioception to sense position. Then we have the special senses of sight, hearing, smell , taste etc via our cranial nerves. We have higher levels of motor function controlling our equilibrium and gait via the inner ear (8th cranial nerves) the basal ganglia and the cerebellum (old brain). All of these systems can be sensed by us and are somewhat under our control. The autonomic nervous system controls our bodily functions and is completely out of our consciousness or control. The brain autoregulates the heart, lungs, kidneys, liver , intestines etc. we cannot command our heart to beat, our lungs to breath, stomach to digest etc. Try holding your breath for 6 minutes. You will not be able to and your brain will make you breath due to CO 2 accumulation. The autonomic nervous system has 2 separate systems working in conjunction, the sympathetic and parasympathetic. In short, the neurotransmitter for the sympathetic nervous system is adrenaline and for the parasympathetic its acetylcholine. The 2 work in conjunction and the sympathetic is essentially our waking system and the parasympathetic system shuts everything down at night when we rest. So heart rate drops to 40s, breathing is 8-10x min, bowel and bladder function cease while we sleep. During day we need these organ on full blast and adrenaline does that. Fright-flight is the term commonly used to describe this. This is a very oversimplified depiction but it helps to understand the problem. The brain has trouble differentiating our internal organs , unlike our appendages for instance. You know left from right but gallbladder problems are referred to the shoulder, angina to the left arm or neck. This is referred to dermatomes that were formed in utero. Dysautonomia or autonomic dysreflexia is the disease of malfunction of this systems . If acetylcholine is released when we stand and gravity pulls blood to our feet, the arteries dilated and heart rate drop . The blood pressure and cardiac output drop and cerebral perfusion drops .. patients get dizzy and can actually have syncope ( pass out). Thats one form of dysautonomia called boss-vagal syncope or neurocardiogenic syncope. The brain is overriding the cardiovascular system. Theres a spectrum of symptoms from mild (palpitation and tachycardia at rest) to severe with cardio-inhibitor -vasodrepressor syncope requiring medications and occasionally pacemaker implants. Parkinsons disease is the most severe form of orthostatic blood pressure (bp drops when go from supine or sitting to standing). Anything more than a drop of 20 mmhg is abnormal and causes symptoms. PD patients will drop 100mmhg when its very severe. So what does this have to do with sharp chest pain in you? Your anxiety and panic attacks are triggering your dysautonomia.. your mind suffers the body will follow . The brain hijacks any and all , chest hurts, pulses quickens, skipped beats extra beats, hyperventilation, stomach cramps, diarrhea, nausea and even vomiting. Nothing is inherently wrong with any of your organs. Thats the brain referring its suffering to these organs . Treat the source. When the stress and anxiety are under control , these symptoms will resolve. Thats why they only occur when you are inside your head at quiet times. You dont feel this at exercise because the body releases endorphins, our natural anxiolytics. This needs to be addressed. A small dose of metoprolol can help ( beta blocker) for the cardiac manifestations. But the source is the psyche . Treat that and all will get better. Thats why people with this problem never have symptoms on vacation when out and about. !!!! As a cautionary note, while anxiety can mimic cardiac chest pain, long standing anxiety and stress can cause premature cardiovascular disease and death. The release of pro- inflammatory, harmful cytokines damage all of our organs. Thats what stress causes. It takes a several decades, but high stress folks dont see their 90s. Stress kills. Plus it robs the joy out of life. So quit worrying about your heart. Its fine. Focus on that head of yours !!! lol All joking aside, if you fix the mental issues the rest will follow. Dont fix it and feel like this for the long haul. And it will eventually get worse. So get get it treated. You got this. Good luck

Nothing!.. do not get caught up in ECG jargon. Those numbers represent the direction of the electrical vectors for p-wave (atrial depolarization) qrs (ventricular depolarization) and t wave (ventricular depolarization). The directional vectors are influenced by various cardiac conditions and pathological states ( hypertrophy, scarring from MI, etc). Those numbers on your ecg represent normal quadrants. But to understand the details and nuances of ECGs requires 3 years of cardiovascular fellowship training. And non specific T waves are just that. Non-specific. It tells nothing and many people with normal hearts have insignificant T- wave changes. Forget the ECG. Its a piece of information thats very nonspecific. I have patients with terrible heart disease and heart failure, who have normal ECGs. And vice versa, those who have really ugly ECGs and absolutely normal heart muscle. Cardiologist rely on echocardiograms images (ultrasound) to evaluate patients for structural heart disease. Because ECG leads measure amplitude and direction of the electrical conduction system of the heart. Those electrical vectors are affected by tissue, bone, etc (obesity, breast size, small patients) and age ( younger have higher amplitude) , in addition to cardiac abnormalities. And lead placement can also make the ECG abnormal. 12 leads are attached to the chest and misplaced leads can give the ecg the appearance of a previous MI So , your ECG is normal, like most 38 year old females. We dont see many abnormalities in young, otherwise healthy, females unless they were born with some form of congenital heart disease. I read between 5-10k ecg per year. More than 80% of those from the ER are completely normal or represent normal variants (like yours). Unless we capture an arrhythmia or do an ECG during an acute cardiac syndrome (MI), most are unremarkable. We dont rely

At age 84 , our blood pressure goals do change. The side effect profile of many medications gets magnified by advanced age. To summarize the blood pressure goals based on the current cardiac guidelines, The ideal blood pressure is 120/80 or less. Pre-hypertension ( borderline high blood pressure) is 121-129. The cutoff is 130/80. Above that is stage 1 hypertension. 140/90 is the old cutoff . Now above 140/90 is stage 2,hypertension (old cutoff is 160/100). When we see patients, if either systolic (upper number) or diastolic (lower number) is above cutoff, then we round up. So 129/92 is Stage 2 hypertension (diastolic > 90). So we treat blood pressure aggressively. The cardiovascular treatment guidelines for hypertension were changed in 2017, because even mild longstanding hypertension leads :,to more myocardial infarctions (heart attacks); more congestive heart failure ; and more cerebral vascular accidents (strokes). Treatment starts with a long acting diuretic (chlorthalidone) and/or a calcium channel blocker (amlodipine). Its also reasonable to start with an angiotensin receptor blocker (losartan) or ARB. This is interchangeable with an angiotensin converting enzyme inhibitor ( lisinopril), particularly if they are diabetic or any form of heart failure. Beta blockers (metoprolol) are first line in patients with a history of coronary artery disease and MI. We often use 2 drugs at moderate doses (for the greater additive/ synergistic defects) ., rather than uptitrate mono therapy with

My mistake. You are female, I misread. One less risk factor and even less likely CAD. But my recs remain the same ..

Too many heart beats sounds like premature contractions coming from upper chambers ( premature atrial contractions) or lower chamber ( premature ventricular contractions). In themselves these are not a serious issue. Stimulants. Sinus meds, coffeine, electrolytes abnormalities can cause them. Anything that increases adrenaline in the body. Also electrolyte abnormalities. This can be related to an underlying problem with the heart muscle (cardiomyopathy), scars (previous MI / heart attacks) , or ischemic heart disease ( plaque blocking coronary blood flow). If you have those underlying conditions, see your cardiologist. The treatment can be watch and wait because they come and go spontaneously. Or medication to slow down the heart ( beta blockers) or true antiarrhythmic medications if they are frequent and symptomatic. The vast majority of the time this resolves with treatment and time. Everyone has them but not everyone feels them ( extra forceful beats if it PvC) . Of course this is a presumption on my part because the sentence the physician told you is very nonspecific. Perhaps he meant an underlying arrhythmia like atrial fibrillation or atrial flutter. I doubt that because he would have treated those conditions. The other possibility is gallop beats or abnormal heart sounds. These are not true extra beats but extra sounds blood makes when it fill a diseased abnormal left ventricle. Again, this would have warranted a much different discussion, work up and treatment. My best guess would be extra beats and you should be fine. As for the treatment of your cancer, the regimen used for colon cancer tends to not result in damage to the heart. In the old days high doses of anthracyclines ( doxorubicin and daunorubicin) for breast cancer and lymphomas, caused dilated weakened ventricles and heart failure. Oncologist are very careful in todays chemo regimens, and I have not seen a chemo induced , new cardiomyopathy in recent memory. The heart is monitored throughout if and when the cancer agent presents cardiac risk. This would have occurred before 2 years and you would have heart failure signs and symptoms ( shortness of breath, fluid build up). Radiation can also damage the heart if its in the x - ray field , which shouldnt happen with colon cancer. Best of the doctors vague explanation, I would be surprised if this is anything serious

You are ok. First , the blood pressure. 130/80 is the cutoff. It said stage I because of the diastolic of 85. No doctor is going to initiate medical treatment for that minimal increase. You can lower it with diet and exercise. The DASH diet for cardiovascular health and low sodium for hypertension ( high blood pressure). Moderate intensity aerobic exercise for 30 minutes 4-5 times a week. You could benefit from some weight loss. You are overweight but not obese. Ideally your weight would be 170-180 for your height unless you were very muscular)muscle weighs more. But 10 lbs of weight loss can lower bp by 5-10mmhg. And diet and exercise another 5-10mmhg. Your physician can order ambulatory BP monitor to follow bp. If you want to do your own . Check it 3x a week at different times and record the numbers. We as physicians would much rather the healthy control of BP in 19 yo and try to avoid meds. After a few months if bp is still high on 3 mo follow up we could initiate a diuretic like chlorthalidone or amlodipine (vasodilator). But meds have potential side effects. Your bp might be ok on follow up. And stop worrying about it. Ideal bp 120/80 or less . You are not that high at all. Relax. Because stress increases bp. You should adapt a healthy lifestyle regardless of BP for overall health. Good luck

Part 1 I agree with your others physicians . Your symptoms are very atypical and not consistent with true angina. Allow me to explain. Angina is a specific type of chest pain related to ischemia (lack of oxygen delivery to cardiac muscle) because of diminished blood flow. The diminished blood flow is caused by atherosclerotic plaque occluding part on the lumen of the coronary arteries. This plaque is the result on longstanding pathological processes, related to heredity and environmental factors (high fat, high carb American diet). The plaque consists of an inflammatory milieu of smooth muscle cells, macrophages and foam cells, fibroblasts, collagen, calcium, inflammatory cytokines, pro- coagulant factors and other free radicals . But the primary ingredient is low density lipoprotein (LDL), which makes up part of our total cholesterol. The LDL circulating in our bloodstream will attach to areas of damage to the inner lining of the coronary artery ( endothelial or intimal layer) , which is one cell thick. This process starts in our late teens and early 20s with the development of fatty streaks on the intimal layer of the aorta. Over time the ldl begets LDL. The plaque adds layers and enlarges. This will happen more rapidly if a person has hyperlipidemia or hypercholesterolemia (disease with elevated levels of lipoproteins due to diminished LDL receptors in the liver to breakdown and metabolize LDL). The plaque cannot enlarge outward to any significant degree because of the muscular layer in the middle of the artery (media) which prevents this progression. So over time ( years, not months) the plaque bulges , then protrudes, into the inner cavity of the artery where the blood flows (lumen). Over the years, as the plaque enlarges, and occludes more and more of the lumen, a patient can begin to develop symptoms. This level of obstruction to the degree of severity to cause symptoms has been studied exhaustively. The cutoff has been determined to be 70%. If the plaque burden obstructs less than 70% , the vast majority of patients will not have symptoms ( angina) with normal activity. Less than 50% wont cause symptoms with high intensity, strenuous workloads. Plaque size greater that 70% can cause symptoms with activity and also results in abnormal stress tests. The symptoms usually progress in an indolent manner over extended months. At first patients report diminished energy levels , with increasing fatigue, lethargy and somnolence. Patients report falling asleep and being exhausted getting home from work. A noticeably differently in functional capacity when compared to 6-12 months prior. Then as the blockage increases in severity, patients will develop dyspnea with exertion ( shortness of breath). Patients complain of being winded just going up one or two flights of steps at work. Then, as the obstruction grows, patients begin experiencing substernal chest pain with exertion or stress. This pain is characterized by pressure or heaviness, like someone is sitting on your chest. The symptoms tend to be at least moderate 5-6/10 , or worse. The pain is associated with shortness of breath, sweating ( diaphoresis) , nausea / occasional vomiting. The pain can radiate to the left arm, the neck or jaw, or both arms (90% specific). The duration is 5-10 minutes and the pain is relieved with rest or SL nitroglycerin. For men , the classic symptoms of angina occur while cutting the grass. They have to take multiple breaks. This is an important part. The symptoms occur with activities, not at rest. The coronary lumen can be blocked with plaque up to 95-99% , and there will be no anginal symptoms at rest. Because its based on supply and demand. As we move the heart has to pump blood to the large muscles of the glutes and legs. To do that work load the heart needs oxygenated blood cells . If theres significant plaque burden , ischemia will occur ( demand exceeds supply) and the pain will stop the activity to protect the heart . The same threshold will of strenuous activity will continually induce the symptoms. The anginal equivalent is repetitive and predictable. It can be induced with stress or anxiety also. If patients stop doing things they wont feel bad. The symptoms dont occur at rest or with minimal activity until patients are having an acute coronary syndrome ( unstable angina or subendocardial MI). If the patients arent very active, so no real pattern emerges, we can do a stress test. Either treadmill or pharmacologic, and with or without nuclear images. If a patient has significant plaque burden of 75% or more, they will stop the treadmill protocol after a few minutes and often have dyspnea and anginal symptoms with ECG changes in the ST segments . These anginal symptoms with exertion are consider typical chest pain or angina. If the symptoms have some of the characteristics of angina , but not others ( cp is sharp , radiates to the right arm, occurs while supine) , the chest pain is call atypical . Lastly , if the chest pain has no characteristics of angina, we term it noncardiac chest pain. This could be secondary to deep muscle strain in the chest wall, gastric reflux, nerve entrapment, stress/anxiety, pleurisy, and upper respiratory tract infections with excessive coughing . In these cases the pain patterns will be different. Most importantly, most other sources occur at rest , or have no changes with exertion and no pattern of occurance. A fixed blockage with heavy plaque burden will continue to cause symptoms with exertion until we dilate the artery more ( long acting nitroglycerin, ca channel blockers, beta blockers ) and reduce the stress /strain on the heart. Medication is the initial treatment but ultimately the patient will need angioplasty and stent deployment to obliterate the plaque volume. When the symptoms have some characteristic of angina but some are atypical , we use an algorithm called Bayes Theorem . With this theorem we look at the symptoms and the risk factors to be determine the pre-test probability of the diagnostic test being abnormal in a patient with the disease. We use screening tests like stress tests to to prove what it isnt . Screening test need high sensitivity ( very low percentage of FalseNegatives ). We dont want a patient with severe coronary disease walking around with a normal stress test . The trade off is higher false positives lower specificity. The risk factors for coronary artery disease are: male gender ; age > 50 for man ; > 60 for a woman; hypertension; hyperchesterolemia; diabetes; smoking; obesity; strong family history in 1st degree relatives (parents/ siblings) ; previous history of coronary disease or its equivalent ( peripheral artery disease, cva/tia/ strokes) . So if an 18 yo marine comes in with chest pain after a 10 mile run described as sharp with no associated anginal qualities , then he needs no further testing. But if his grandpa comes in complaining of worsening shortness of breath doing his woodwork and gardening along with chest tightness when he walks up a hill, we will not waste time with a stress test. Especially if he already has coronary stents or bypass of previous MI. We will schedule an angiogram urgently and optimize the medication. The marine has less than 10% chance of having coronary disease and has no risk factors. Give him ibuprofen. Even if he had an abnormal stress we wouldnt believe it and call it false positive. In grandpa his pre test probability is > 90 %. So no stress test and we proceed directly with angiogram. If his stress test was negative, I wouldnt believe it . Then we have the middle age female , similar to you. They are between 10 and 90. So we consider the stress test for screening. We will discuss this application to you in part 2 . Tomorrow..

That is a normal echocardiogram for a relatively young, healthy patient. I did extra training in echocardiogram and got board certified. Few cardiologist do that. Low normal EF 50-55% is still normal. We see this all the time in 20 yr olds. The heart is strong so it doesnt need to increased systolic squeeze to maintain cardiac output. All of your chambers are normal sized and all the valves are normal. I read 200 echos a month and you learn to read between the lines. I can tell by everything else being normal, they undercalled the EF. Its very subjective and if 10 cardiologist read your study there is a 5-10% difference in reporting. That has been proven and documented in cardiac literature. Yours is a normal study . Same thing with aortic root diameter. 2 d echo is very user dependent. If the calipers arent just right and the images were obtained correctly, its not uncommon to have standard deviations between interpretation of 3-5mm. That makes a size of a pinhead or thickness of a quarter. Its not a very accurate measure of the root or ascending aorta. We arent concerned about something like aneurysm until diameter is > 4-4.5 and surgery until its 5 or greater. They can recheck echo in a year. If its normal again then its usually nothing. If you are still concerned , have them order a CT scan with aortic angiography. That study (or MRA) is more accurate . For echocardiogram, a trans esophageal echo is good standard. We sedate you and put probe down throat. This has far superior spatial resolution then trans thoracic echo ( much less tissue artifact). Mostly RELAX

Unfortunately, your symptoms could be an anginal equivalent , related to significant underlying coronary artery disease. Your age is just one risk factor (the others: hypertension, Diabetes, hyperlipidemia, smoking, personal history of CV disease, and a strong family history of CV disease in first degree relatives), but it appears you have been fairly healthy. The symptoms are atypical, occurring in supine position and less pronounced when performing ADL. Atherosclerotic (lipid rich) plaque in the coronary arteries will induce exertional anginal symptoms when the lesion occludes more than 70% of the arterial lumen. This degree of stenosis would also result in an abnormal perfusion defect during a nuclear stress test. However, I have had many patients over the years with multiple 95% stenosis in more than one coronary artery. Also, subtotaled 99% stenosis with delayed string-like flow. But not one of those patients had symptoms at rest. Classic angina is induced with exertion or stress/anxiety, and it is relieved with rest and/or sublingual nitroglycerin. You had symptoms at rest to a much greater degree than with exertion, the opposite of what would be expected from a significant coronary stenosis. The symptoms you described would be considered atypical ( not classic, but could represent her anginal equivalent). Atypical symptoms occur most often in the elderly population, with female gender, and in patients with autonomic neuropathy ( long standing diabetes). These patients experience exertional fatigue, lack of energy and dyspnea with exertion. Their is also a rare form of angina , called angina decubitus, which occurs in the supine position and not so much with activity. While the pattern of your symptoms wasnt classic, the qualities were worrisome for true angina. Heaviness, and pressure sound like someone with underlying CAD. The biggest clue was the fact that the discomfort radiated to both shoulders/upper arms. That is 95% specific for true angina from underlying high grade atherosclerotic plaque. You should be treated medically now ( asa, nitrates, beta block er, statin) and undergo urgent nuclear stress testing or invasive coronary angiography. Assuming the angiogram was done and came back negative, What else could induce such symptoms, in this pattern? The answer is gastrointestinal reflux, with esophageal spasm. The internal organs in the thorax (lungs, heart ) are innervated by the autonomic nervous system, via the 10th cranial nerve, the Vagus. Unlike skeletal muscle, the brain cannot distinguish between the esophagus and the heart. The heart sits on top of the esophagus and the hydrochloric acid in the stomach is .1% molar. Unlike the stomach, the esophagus doesnt have the protective mucous and goblet cells. When the acid refluxes and hits the esophagus, it will spasm. This pain can be quite severe and mimic true angina in every way , except one. The pattern. Both respond to nitroglycerin and both can feel like burning or pressure, with radiation. However reflux is exacerbated after a meal or lying down. The effect of gravity is lost in the supine position. And the brain, as mentioned, cannot tell the difference between these organs, referring the symptoms to what it does know, skeletal muscle ( arms). The patient would benefit from nitroglycerin, long acting. Bland diet and weight loss. Mostly, proton pump inhibitor therapy . Their are long term complications from chronic reflux (Barrett esophagus) but Short term the risk is low. In your case , I would treat both conditions and cycle the cardiac enzymes, ecg , echo. Stress test is an option but have a low threshold to perform angiography if the stress is even mildly abnormal. Coronary angiography/ coronary catheterization is a low risk procedure and takes less than 30 minutes. when done through radial access the complication rate is <1%. But its the gold standard for diagnosing and treatment of CAD. Also , intracardiac Pressures in the LV can be measured and LV function can be estimated. If the angiogram were negative, the patient will also get peace of mind. The pt can be referred to GI for EGD as an outpatient.

The only thing to avoid with a stent in the coronaries or peripheral circulation that is absolute, is dont stop taking dual platelet inhibitors ( aspirin plus either clopidogrel prasugrel or ticagrelor). The stents are at risk for thrombosis ( clots) early in the first 6 months and stent restenosis with recurrent plaque later. We recommend at least a year for drug-eluding stents (coated with immunosuppressives like sirolimus) and a faction of cardiogists ( including me) believe in 2 years up to indefinite therapy , as long as its tolerated. Bare metal stents with no drug coating

Good questions. The most important things to avoid in patients with hypertension (high BP) are things we ingest.. Sodium ,and food high in sodium content, is the number 1 offender . Na will cause elevated BP by several mechanisms , particularly effects on the renin - angiotensin-aldosterone feedback loop ,involving the kidneys. Also direct effects on the vascular endothelium occur and effects on the heart with increased wall stress / strain and the release of vasoactive hormones (BNP, vasopressin) . The last organ involved in sodium regulation and BP control, is the brain. The brain can auto regulate blood flow in times of shock and hypotension (low bp). Brain can cause vasoconstriction or dilatation via the autonomic nervous system and effect BP via hormones from the hypothalamus-pituitary gland- adrenal gland axis (negative feedback loop) . After sodium excess , the next offenders would also involve ingested of certain foods /products/ chemicals , such as alcohol, steroids and non steroidal anti-inflammatory meds(ibuprofen) . Steroids lead to sodium retention and change vascular tone. NSAIDS block prostaglandin effects on the afferent arterioles in the glomerulus of the nephrons , an additive effect to the negative impact of angiotensin on renal blood flow and perfusion. After the brain and heart, the kidneys have the next highest oxygen requirement, metabolic rate and the next highest percentage of the cardiac output auto- directed to its perfusion. These 3 organs, and the adrenal glands atop the kidneys , are the major players in BP control ..so it goes without saying that foodstuffs and drugs that have deleterious effect on these organs will effect BP. Many effective BP meds achieve lowered bp by its effect on these organs. Some chemicals ( , cocaine/meth / diet pills/ adderal )cause intense vasoconstriction with elevated HR. But any prescription drug or health product can potentially effect BP by effecting the above mentioned organs. Along with sodium content, alcohol , medications and illicit drugs, nicotine has the effect of raising bp by vasoconstriction. Other causes of elevated BP include intense pain, illness , stress/anxiety , and , the most common cause of refractory hypertension, medical noncompliance. There can be secondary causes of elevated BP such as fbromuscular dysplasia, renal art stenosis, adrenal hyperplasia (conns syndrome) or nodules , neuroendocrine tumor ( pheochromocytomas of the pancreas) and pituitary adenomas ( Cushings disease) ., Obesity , untreated sleep apnea and sedintary lifestyle. Like many things , bp can be lowered in many by non medical treatment modalities. The Dash diet, weight loss,wearing cpap, abstinince from alcohol tobacco and illicit drugs. Intervention or surgery for secondary causes. Aerobic exercise for 30 minutes 4-5 x week with mod intensity will lower bp by 10 mmhg. and medical compliance when meds are required to get to goal bp of less than 130/80. Ideal is 120/80. Stage 2 is >140/90. Because of long term deleterious effect of chronic hypertension on the cardiovascular system (MI,CHF, CVA), guidelines were changed and goals lowered in 2017. After all , Hypertension is the most common disease in this country (116 mil), so the greatest benefit on the population can be achieved by optimization.

Well technically speaking, deploying a stent in a coronary artery, or any other artery for matter, is not considered a true surgical procedure. We do our work through catheters after we insert sheaths in the radial artery of the wrist or the femoral artery of the groin. It all starts with a needle puncture. And if it is a straightforward stenosis in a favorable location of the artery (a mid-RCA 80% discreet lipid filled soft plaque) the whole procedure might take 30 minutes or less. And most patients go home in a couple of hours. Complex lesions in the ostium of the left-sided coronaries (LAD, LCX) are more high risk and the patient may get kept in the hospital overnight. Hard plaque made predominantly of calcium , or completely occluded arteries (CTO), are much riskier with a higher complication rate because we have to drill/chisel through the lesion with an atherectomy device. We use clinical judgement, but would lean towards keeping those patients in the hospital overnight. Each case is a little different, but most patients can go swimming within a day or two. Particularly an elective, uncomplicated, outpatient case in a stable patient done radially with no significant co-morbidities and no procedural complications. The patient who is admitted with an acute coronary syndrome or acute infarction ( heart attack), with or without hemodynamic instability, may be taken to the Cath lab emergently , or at least urgently the next morning, will be in the hospital longer. They have some degree of acute muscle damage even when the procedure is successfully. Their heart damage was the result of complete thrombotic obstruction of the artery as a result of acute plaque rupture (platelets in the bloodstream aggregate or clump over the site of the plaque rupture which then completely occludes the artery). Once we re-establish blood flow by percutaneous intervention and stent deployment, the flood of blood to the ischemic portion of cardiac muscle causing myocardial stunning . That portion of the muscle will be dysfunctional for up to 6 weeks. Most eventually normalize. But the recovery from even a small to moderate myocardial infarction is 4-6 weeks. So they wont physically be able to swim after discharge for several weeks. They dont have the energy or stamina. The actual procedure doesnt determine when they can swim, but the clinical scenario. In general, from a wound and procedural standpoint, a patient could swim within 2 days of discharge ( maybe even the next day).

No, you should not drink alcohol if you are experiencing palpitations. Alcohol is known to adversely affect the cardiac electrical conduction system. The mechanisms arent important. What is important is that binge drinking, in particular, can cause atrial fibrillation, even in younger patients. Its called the Holiday Heart syndrome. Atrial fibrillation comes with its potential complications, including thromboembolic CVAs. The thrombus, blood clot, that form in the left atrial appendage can leave the heart and travel up the carotid arteries to the middle cerebral artery. Eventually they obstruct the small arterioles and capillaries in the temporal- parietal lobes, leading to strokes that can paralyze one side of the body. ( hemiparesis) and affect speech permanently (Aphasia). Atrial fibrillation also causes sustained rapid heart rates or tachycardia, with ventricular rates as high as 150-180 bpm. The myocardium (heart muscle) can not sustain normal systolic function (contraction) if these rates persist for more than a couple of days. This can lead to tachycardic-induced cardiomyopathy and congestive heart failure. Atrial fibrillation is not the most common cause of palpitations. Most palpitations are related to premature ventricular contractions or PVCs, extra strong beats originating from electrically excitable myocardial cells in the ventricles. Alcohol can cause PVCs or exacerbate pre-existing ectopic beats from either chamber, including premature atrial contractions orPACs. To diagnose the cause we generally have the patient get an ecg in clinic then check electrolytes levels. If necessary they can wear a monitor for several days. The root cause is often malfunction of the autonomic nervous system and elevated levels of neurohormones, such as norepinephrine (an adrenaline analog). Alcohol will aggravate this type of automaticity and hyper excitable tissue. The treatment is usually beta blocker therapy (metoprolol) for most causes of palpitations. These drugs slow down heart rate and contractility and relax the excitable foci in the myocardial tissue. But avoidance of stimulants ( Sudafed, diet pills ADD meds, excessive caffeine), alcohol , and offending prescription drugs ( albuterol inhalers, steroids) are a necessary part of treatment.

The quick answer is yes, within reason.1-2 cups a day, but after the blood pressure is controlled. Consistently below 130/80 on average with a goal of 120/80 or less. Not below 100 systolic with the risk of presyncope. Of course decaffeinated coffee is fine. Different patients are effected by caffeine to various degrees. Based on tolerance, the dose (brewed coffee is approximately 150mg) , and individual physiology. Most patients require more than one medication (US pts avg 2.4 meds). Beta blockers would mitigate the stimulant effect of caffeine on heart rate and contractility. Over time the patient will find that middle ground where a cup of coffee has little effect on pulse and BP. The effect of caffeine is transient. Its short acting with beverages and the effect on blood pressure will be over in a couple of hours. So , if you have high BP and really like coffee, take your blood pressure and morning meds. Drink your brew 30-60 mins later and check pressure again at 30/60/90 mins. After a couple of hours it should be at baseline. You can always have your physician increase the dose or add another Med if bp is staying elevated. I have high BP controlled on 2 meds and caffeine has little effect. I drink a 32 oz ice coffee. But Im tolerant to the effects after so many years. Youll figure out your own pattern and adjustment. As long as you dont drink excessively, you shouldnt have to go without coffee. I know I wouldnt K

Not unless its mildly elevated. The only 2 diets the ACC/AHA promote as heart healthy are the Mediterranean and DASH diets. They are very similar but DASH is low sodium for patients with hypertension (high blood pressure) . Its hard for patients to change their lifestyle and eating the average American diet is high is salt, fat and carbs. But if the DASH diet is followed religiously then the cardiovascular system is protected from future atherosclerosis and coronary events. These 2 diets have shown positive morbidity and mortality benefits over the long haul. The diet can lower blood pressure approximately 10 mmhg. The diet combined With moderate intensity exercise for 30 minutes 4-5 x week ( walkers do better than runners) and weight loss ( if overweight or obese) will improve that to 15-20mmhg. But thats following a strict regimen and significant changes in habits. Also we cant for get smoking cessation. That also lowers BP. So if all those modifications of lifestyle are adopted and stuck with day in and day out , its possible to avoid medication. Possible, not likely. But the medication I use for blood pressure also has cardiac benefits (beta blockers, acei, arbs) . Regardless of whether bp reaches a goal of less 120/80, the cv system benefits from those lifestyle changes. Its better to do the lifestyle changes and medication to reach the goal of BP, than to worry about needing to take medication. Cardiac meds have shown cv benefits in 100s of randomized trials in hundreds of thousands of patients. I wouldnt hesitate to prescribe these medications if necessary. I have high bp and take some of these myself. The benefits of controlling BP by all means is vital. Even mildly elevated BP can cause increased strokes, heart attacks and heart failure later in life. So think first of getting to the goal BP, and use a holistic approach. Diet, exercise, weight loss if needed, and smoking cessation for those who smoke. Then meds if needed. In my experience most patients would rather medication rather than strict wholesale lifestyle changes. But if you can do it the benefits go beyond just blood pressure control. Sometimes , no matter how stringent the diet and exercise, meds will be needed. Genetics play a large role. And race (blacks have higher bp and younger ages), stress levels and other meds (ibuprofen, steroids) . Dont forget alcohol. Binge drinking on weekends raises BP for 2-3 days after. 1-2 glasses red wine are ok. The beer and harder liquor have no benefits and harm in other ways ( bp, sugar intake, liver toxicity , and less healthy lifestyle). If bp is near 130, dash diet alone could do it. Give it 3 months and have your doctor re-evaluate. Again, if it doesnt quite get it done , a medication or 2 is worth reaching the goal BP. But stay on the diet and live longer ..

The more I learn about covid the less I know ! The best answer I can tell you is that covid can do anything to anyone at anytime.. sounds like a cop out but Im being honest , mostly. I should have said covid can do anything bad to anyone. No good comes from it. I had two patients get arrhythmias from covid vaccination, that stand out because of the complications. Both had atrial fibrillation and thromboembolic complications. Covid is an endothelial/ interstitial disease, infecting and inflaming the inner lining of blood vessels and organ tissues. Take the lungs, the virus attacks the lining in the small capillaries and arterioles where air crosses into the blood. Thats how oxygen gets from the air we breath and attached to the iron on the hemoglobin molecule on our red blood cells. That thin membrane of interstitial tissue becomes inflamed and leaky and causes the alveoli (air sacs) to become secondarily filled with fluid so their is little air exchange. The result is clinical pneumonia with low oxygen saturation (hypoxia ). This inflammatory state is hypercoaguable and blood clots form in the lungs and peripheral vascular circulation ,as in DVTs and pulmonary emboli. With the heart , covid can infect the lining ( endocardium) and the middle muscular layer ( myocardium) . This can lead to arrhythmias if the endocardium is affected in the electrical conduction system. The tissue inflammation can also cause myocarditis if the muscular myocardium becomes involved . .this can result in Atrial Fibrillation. A fib is the most common, but not the only arrhythmias noted to be the result of this process. Svt and other atrial tachycardia arrhythmias can occur. Sinus tachycardia (fast heart rate) is seen most commonly seen tach rhythm. Bradycardia, and slow rhythm like those of Heart block, and ventricular arrhythmias are less common. I have not personally seen a lot of primary cardiac manifestations of covid. In my clinic or in the hospital. Most of the hospital patients were for respiratory illnesses, including myself. I contracted pneumonia from covid in December of 2020. I had bilateral pneumonia with a pulmonary embolism that caused me to crash from a respiratory standpoint. Thankfully I was in good shape for my age, But I was still on oxygen for another month and missed 3 months of work - after 10 days in the icu ..I wasnt fully back to myself for almost a year . As for the 2 patients of mine that developed a-fib, both were after the maderna vaccine in 2021. They didnt actually get the virus. Pt A had a fib with a rate up to 170. Went into heart failure and had an embolus to his left foot. He had surgery and almost lost his leg. I did a trans esophagus echocardiogram and shocked him back into a regular rhythm. Sinus rhythm was maintained with anti arrhythmic meds. Angiogram confirmed no significant atherosclerosis of his coronaries..It took me a year to get him back to his normal baseline. But he was 63 yr old. Pt B was 25 years old. He got septic after the first dose of maderna and had high fever. After the second dose he had a fever of 105 and developed myocarditis , dilated cardiomyopathy with chf . and he secondary went into a fib from the dilated heart chambers. He developed a thrombus in the left ventricle at the apex ,or tip of the heart , that wasnt squeezing (mural thrombus). A part broke away and he a embolism to the vertebral arteries and a posterior cva (stroke) - involving the occipital lobe (part of the brain that has to do with vision). He lost peripheral vision in both eyes ( hemianopsia). I was able to convert him out of a fib with medication .. but he still has dilated weak heart and most likely has permanent peripheral blindness .. so with covid infection anything can happen. Myocarditis would be the most severe manifestation.. which could cause atrial fibrillation or even ventricular tachycardia. A fib and other arrhythmias can be caused directly by the virus and not be secondary to chf. Or even the older original version of the vaccines. The good news is like most viruses , covid has attenuated to the point where its no different than the flu, and no more virulent. I havent seen or heard of arrhythmias from covid in over a year. We have had very few respiratory failure patients or serious pneumonias. The atypical chest pain and shortness of breath that was prevalent ( due to dysautonomia) , has all but vanished ..

Technically alcohol has no effect on coronary disease or coronary interventions. In face there is some evidence that moderate alcohol intake is beneficial. I would never recommend alcohol beyond a glass of red wine at evening meals. If a patient has angiography followed by percutaneous Intervention with balloon angioplasty and stent placement , I would not let them drink alcohol that first night because of the sedation and pain meds we give for the procedure (versed and fentanyl ). That interaction can lead to adverse reaction which can be quite serious. But beyond that, a couple of cocktails or beers in the evening has no effect on the stents. But I think drinking excessively is not acceptable for many reasons. Heavy alcohol in a chronic fashion damages other organs which could eventually cardiac complications. Some are alcohol related dilated cardiomyopathy, new