“Are they panic attacks or is it my heart?”

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..