I am a 33 yr old female and I swear I have heart issues. I have had so many test done for my heart and everything has come back 100% normal.
i have had countless number of EKG's
I have a 48 heart montior
I had a echo of my heart.
my bp is a little high (bottom number in the low 80's)
my cholesterol total is 166.
I do suffer from panic/anxiety and my Dr (bless his heart he is awesome) says all the things I feel is related to my panic not heart.
Is there really anything else they could do to test my heart or did I pretty get everything?
My doc said he wouldn't send me for a cardic cath cuz everything else was fine. Yes I do take meds to my panic attacks. If you have had all those tests already & they have all come back negative then considering also you suffer from an anxiety disorder i would almost garuentee those symptoms you are experiencing are panic related. I myself have suffered an anxiety/panic disorder & for years i was convinced something was wrong with my heart, i think it is very common for people with anxiety to also think the same. I have had symptoms like chest pain, tightness, palpitations, even felt like the pain is going down my harm & still the tests i have had done are negative. Try & trust in what the doctors tell you & focus more on something else & less on your symptoms, if you don't give them any attention, gradually they will go away CALM YOUR SELF DOWN AND FIND SOMETHING ELSE TO DO BESIDES WORRY. IF YOU KEEP LOOKING SOMEONE WILL CUT YOU OPEN JUST FOR THE $$$ yep - your heart sounds quite healthy. Those dang panic attacks could make you feel youre having a heart attack. hhhhmmmm-when was the last time you had a nice hot bubble bath with soft music, low lights and candles? I have a similar situation - my cardiologist says everything is fine and yet I still get the classic symptoms of a heart attack. the last time i went to the nearest er and they kept me overnight and then my cardio doctor came in the next day and said go home your fine. (this was after another bout on the tread mill) bottom line - whenever i get the chest pain etc I immediately take some aspirin and eventually it goes away. needless to say my medical bills have sharply decreased.
ps - now is the time to get some life insurance - because once they diagnose you with a heart problem is almost impossible to get and very expensive. Celexa. It works. And have your doc test your thyroid function. Low functioning thyroid can cause anxiety, even if it is just low and not a deficit. And see if you can get a sleep study done, sleep apnea can also cause heart symptoms, along with nightmares, anxiety, and daytime fatigue. Are you taking anything for your anxiety/panic attacks? Are you seeing a counselor? Panic attacks and anxiety can plague you until you find a healthy way out of it. Counseling and perhaps medication can help you on your way. If anything, you should adamant with your doctor about recommending a counselor or psychiatrist because untreated anxiety can make even minor illnesses much worse. Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a disease state that occurs when the blood supply to a part of the heart is interrupted. The resulting ischemia or oxygen shortage causes damage and potential death of heart tissue. It is a medical emergency, and the leading cause of death for both men and women all over the world.[1] Important risk factors are a previous history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, any previous episodes of abnormal heart rhythms or syncope, older age- especially men over 40 and women over 50, smoking, excessive alcohol consumption, the abuse of certain illicit drugs, high triglyceride levels, high LDL ("Low-density lipoprotein") and low HDL ("High density lipoprotein"), diabetes, high blood pressure, obesity, and chronically high levels of stress in certain persons.
The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation). The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction.
Classical symptoms of acute myocardial infarction include chest pain, shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom. Patients frequently feel suddenly ill. Women often experience different symptoms than men. The most common symptoms of MI in women include shortness of breath, weakness, and fatigue. Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms.
Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, glyceryl trinitrate and pain relief. The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray and blood tests to detect elevated creatine kinase or troponin levels (these are chemical markers released by damaged tissues, especially the myocardium). Further treatment may include either medications to break down blood clots that block the blood flow to the heart, or mechanically restoring the flow by dilatation or bypass surgery of the blocked coronary artery. Coronary care unit admission allows rapid and safe treatment of complications such as abnormal heart rhythms.
[edit] Epidemiology
Myocardial infarction is a common presentation of ischemic heart disease. The WHO estimated that in 2002, 12.6% of deaths worldwide were from ischemic heart disease.[1] Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries.[2]
In the United States, diseases of the heart are the leading cause of death, causing a higher mortality than cancer (malignant neoplasms).[3] Coronary heart disease is responsible for 1 in 5 deaths in the U.S.. Some 7,200,000 men and 6,000,000 women are living with some form of coronary heart disease. 1,200,000 people suffer a (new or recurrent) coronary attack every year, and about 40% of them die as a result of the attack.[4] This means that roughly every 65 seconds, an American dies of a coronary event.[5]
[edit] Risk factors
Risk factors for atherosclerosis are generally risk factors for myocardial infarction:
older age
male gender[6]
cigarette smoking
hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein)
diabetes (with or without insulin resistance)
high blood pressure
obesity[7] (defined by a body mass index of more than 30 kg/m2, or alternatively by waist circumference or waist-hip ratio).
Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.[8] Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.[6]
Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.[9] To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.[9]
Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.[10]
Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[11] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes.[11] Moreover, some drugs for MI might also reduce CRP levels. [11] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease.[12] Whether CRP plays a direct role in atherosclerosis remains uncertain.[11]
Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.[13] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.[14] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;[15] thus, periodontitis may mediate its effect on MI risk via other risk factors.[16] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.[17][18] A role for specific periodontal bacteria has been suggested but remains to be established.[19]
Baldness, hair greying, a diagonal earlobe crease[20] and possibly other skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.[21]
[edit] Pathophysiology
A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream.Main article: Acute coronary syndrome
Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiographies reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form a cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[22] As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which is particularly bad for the patient experiencing acute myocardial infarction.
The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.
[edit] Causes
Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs.[6] Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit.[6] For those in poor physical condition, the rate differential is over 35-fold higher.[6] One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.[6]
Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[23] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[23] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[24]
[edit] Classification
Classification of acute coronary syndromes.[25]Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).
Depending on the location of the obstruction in the coronary circulation, different zones of the heart can become injured. Using the anatomical terms of location, one can describe anterior, inferior, lateral, apical and septal infarctions (and combinations, such as anteroinferior, anterolateral, and so on).[26] For example, an occlusion of the left anterior descending coronary artery will result in an anterior wall myocardial infarct.[27]
Another distinction is whether a MI is subendocardial, affecting only the inner third to one half of the heart muscle, or transmural, damaging (almost) the entire wall of the heart.[28] The inner part of the heart muscle is more vulnerable to oxygen shortage, because the coronary arteries run inward from the epicardium to the endocardium, and because the blood flow through the heart muscle is hindered by the heart contraction.[27]
The phrases transmural and subendocardial infarction used to be considered synonymous with Q-wave and non-Q-wave myocardial infarction respectively, based on the presence or absence of Q waves on the ECG. It has since been shown that there is no clear correlation between the presence of Q waves with a transmural infarction and the absence of Q waves with a subendocardial infarction,[29] but Q waves are associated with larger infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or absence of Q-waves also has clinical importance,[30] with improved outcomes associated with a lack of Q waves.[31]
The phrase massive attack is not an official medical term.
[edit] Symptoms
Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest).
Back view.The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.[32] Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn. Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.[33] Other conditions such as aortic dissection or pulmonary embolism may present with chest pain and must be considered in the differential diagnosis.
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. Loss of consciousness and even sudden death can occur in myocardial infarctions and are poor prognostic indicators.
Women often experience markedly different symptoms than men. The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.[34]
Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.[35]
Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms.[36] These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. A silent course is more common in the elderly, in patients with diabetes mellitus[37] [38] and after heart transplantation, probably because the donor heart is not connected to nerves of the host.[39] In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[37]
[edit] Diagnosis
The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage).[40] A coronary angiogram allows to visualize narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed on admittance to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction and are sometimes performed in equivocal cases.[41] Technetium and thallium can be used in nuclear medicine to visualize areas of reduced blood flow and tissue viability, respectively.[41][42] Technetium is used in a MUGA scan.
[edit] Diagnostic criteria
WHO criteria[43] have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
Clinical history of ischaemic type chest pain lasting for more than 20 minutes
Changes in serial ECG tracings
Rise and fall of serum cardiac enzymes (biomarkers) such as creatine kinase, troponin I, and lactate dehydrogenase isozymes specific for the heart.
The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.[25] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
[edit] Physical examination
The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38鈥?9 掳C). Blood pressure may be elevated or decreased, and the pulse can be become irregular.[44][45]
If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.[44][46]
12-lead electrocardiogram (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL.
[edit] Electrocardiogram
The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture.[47] It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring.[48] It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle, and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.[47] The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.[49] The 12 lead ECG is used to classify patients into one of three groups:
1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
2. those with ST segment depression or T wave inversion (suspicious for ischemia), and
3. those with a so-called non-diagnostic or normal ECG.[50]
A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation.[51] In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction.[52] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.[53] The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.[50] This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients.[54] In addition, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.[55] The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.[56][57][55]
Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of acute myocadial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.[58] The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.[59]
The presence of ST segment elevation distinguishes between:
STEMI ("ST-Elevation Myocardial Infarction")
NSTEMI ("Non-ST-Elevation Myocardial Infarction") -- diagnosed when cardiac enzymes are elevated. That doctor that is giving you sympathy isnt helping you one bit. Find a doctor that gives straight forward direction, and a direction you might not want to hear.
I suggest you get yourself some kind of a challenging job and put forth your energies to something useful. That cured a friend of mine from panic disorders such as yours. As soon as this lady got involved in her challenging catering job, GONE was the panic disorders, she grew up!!! The nonsense left her and she now lives a happy and rewarding life.
Thanks to a doctor that was straight forward first off, and second she took advice she didnt at first like to hear.
Rid of that doc he is taking your money and doing you no good. Just because he makes you feel good doesnt mean hes worth a plug nickel. Your doctor has checked out your heart, it seems you are dealing poorly with your panic attacks which can almost seem identical to heart problems. But, if you trust your doctor,forget about your heart and take your anxiety meds as prescribed and try to find something else to occupy your mind.
Good luck and good health. |
