Consider the following medical report that includes the patient's historical health records. Use it to predict the disease that the patient is high likely exposed to. 

 Medical Report: allergies: patient recorded as having no known allergies to drugs attending: chief complaint: chest pain major surgical or invasive procedure: -attempted ventricular tachycardia ablation -endotracheal intubation history of present illness: this is a 68 y.o. male with past medical history of mi in s/p ptca at as well as aplastic anemia, dm, and pvd who presented on the day of admission with approximately one hour of chest pain. this pain did not start with exertion as the patient was just walking around his house when he noticed some pain under his sternum. at first, he thought this was most likely heartburn so he took a couple of tums and then went to lay down for a while. unfortunately, after about an hour he was continuing to have this pain, which continued at a five out of ten level and was beginning to radiate into his right shoulder. he was not diaphoretic or short of breath at rest. he described this pain as very similar to his previous cardiac pain but less severe. when the pain did not go away after rest he became concerned for a problem and called the ambulance to take him to this hospital. in the ed initial vital signs were 75, 145/84, rr 15, o2 sat of 96% on 4l. he had an ekg which showed possible st segment elevations and t wave inversions in v3-v5 that remained stable during his time in the ed. initial cardiac enzymes revealed a troponin of 0.74 and cpk of 155 and mb of 6. other remarkable lab values at the time included a cr of 2.2 (up from his baseline of 1.7) and a platelet count of 101. he was given aspirin, clopidogrel, and started on ntg and heparin gtt. his pain resolved early in his ed course and did not recur. the cardiology fellow was consulted and felt though the patient was most likely having an nstemi that he did not need urgent cath so mr. was admitted to the service for management with early cathterization and revascularization planned in the next 24-48 hrs. epifibatide was initially held due to concern about his thrombocytopenia and bleeding risk. past medical history: 1. diabetes mellitus type 2 2. hypertension 3. coronary artery disease s/p balloon angioplasty in 4. peripheral vascular disease s/p r fem- bypass in , 5. s/p right carotid endarterectomy in ; left carotid artery completely occluded but asymptomatic 6. s/p right 5th toe amputation in social history: he is retired. he worked as a maintenance worker at for 25 yrs. he is widowed but has a son and daughter-in-law in town who he stays in close touch with. he lives by himself in poor financial circumstances. he has smoked one and a half packs of cigarettes/day for at least 50 years. he denies alcohol or other drugs. family history: his mother and sister have diabetes mellitus type two. many members of his family have hyptertension. physical exam: on admission: vs: t 97.4, bp 144/87, hr 75, rr 22, o2 sat 100% on 4l gen: this is a chronically ill appearing elderly male in nad heent: sclerae anicteric, perrl, oropharynx benign without petechiae or bleeding neck: supple, jvp at 1 cm above the clavicle, carotid bruit on right side cv: rrr, no m/r/g appreciated, nl s1 and s2 pulm: ctab w/ few crackles at the bases; no wheezes, rhonchi, or rales abdomen: soft, nt, nd, bs+, no masses or hepatosplenomegaly appreciated extremities: cold but not cyanotic with with trace edema bilaterally pulses: dopplerable dp and pt pulses bilaterally, 1- radial pulses, no palpable carotid pulses neuro: a&o *3, responds appropriately to queries, cnii-xii grossly intact, strength 5/5 in all extremities on discharge, exam not significantly changed from admission except for in the following ways. at discharge all vital signs stable with oxygen saturation greater than 93% on room air. no jvd was appreciated. lung exam without crackles, wheezes, rhonchi, or rales on auscultation. no edema noted. pertinent results: <b><u>laboratory results</b></u> on admission: wbc-4.8 rbc-2.53* hgb-9.2* hct-27.1* mcv-107* plt ct-101* ----------neuts-40.7* lymphs-54.1* monos-3.1 eos-1.9 baso-0.3 pt-14.0* ptt-28.8 inr(pt)-1.2* glucose-226* urean-34* creat-2.2* na-132* k-3.9 cl-95* hco3-20* angap-21* on discharge: wbc-3.2* rbc-2.60* hgb-8.8* hct-25.9* mcv-100* plt ct-100* pt-13.4 ptt-35.3* inr(pt)-1.1 glucose-96 urean-33* creat-1.9* na-137 k-4.2 cl-105 hco3-22 angap-14 cardiac enzymes (ck-mb-tropt) 06:55pm 155-6-0.75 01:18am 158-9.7- 0.98 06:35am 172-8- 1.29 11:57am 158-7-1.19 06:32am 119-5-1.06 <b><u>other studies</b></u> ekg on : sinus rhythm with q waves in leads ii, iii and avf consistent with inferior myocardial infarction of indeterminate age. st segment coving in leads v3- with associated t wave inversions consistent with evolving anterior injury pattern. multiple ventricular premature beats. no previous tracing available for comparison. cxr on : impression: there is diffuse pulmonary edema. there is likely a right pleural effusion possibly a small left pleural effusion. a more consolidative process in the right lung base cannot be excluded. the heart appears relatively enlarged even accounting for patient and technical factors which would represent an acute change. repeat radiography following appropriate diuresis is recommended to assess for underlying infection. echocardiogram on : conclusions the left atrium is mildly dilated. there is mild symmetric left ventricular hypertrophy. the left ventricular cavity is moderately dilated. there is an inferolateral basal left ventricular aneurysm. there is severe regional left ventricular systolic dysfunction with akinesis of the mid to distal anterior septum, basal inferior and inferolateral segments, severe hypokinesis of the remaining segments with sparing of the basal septum. overall left ventricular systolic function is severely depressed (lvef= 15-20 %). right ventricular chamber size is normal. with depressed free wall contractility. the aortic root is mildly dilated at the sinus level. the aortic valve leaflets (3) are mildly thickened but aortic stenosis is not present. no aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. mild (1+) mitral regurgitation is seen. there is an anterior space which most likely represents a fat pad. impression: moderately dilated left ventricle with severe regional dysfunction consistent with ischemic heart disease (multivessel). brief hospital course: 68 year old gentleman with history of coronary artery disease s/p mi as well as diabetes mellitus, peripheral vascular disease, and aplastic anemia presenting with chest pain. 1) nstemi/cad: given the patient's multiple risk factors and ekg changes he was diagnosed with presumptive acs on arrival to the ed and thus was almost immediately given aspirin and beta blocker and started on nitroglycerine. his pain resolved after receiving ntg and never recurred. he was also started on heparin. after his first set of cardiac enzymes returned positive the on-call cardiology fellow was contact and made aware of the patient. s/he recommended against epifibatide given the patient's thrombocytopenia and indicated that the patient did not need urgent cathterization. the patient was admitted to the cardiology service with plan for cardiac catheterization in the next 24-48 hours. the patient was then transferred to ccu for sustained vt (see below). repeat cardiac enzymes continued to show flat ck's and echo showed significant wall motion abnormalities suggesting this was a subacute presentation of a myocardial infarction. this indicated less benefit from immediate catheterization and given development of decompensated heart failure and need for intubation (see below) as well as acute renal failure the decision was made to postpone catheterization until after kidney function had normalized. the patient will also have stress perfusion study prior to catheterization as echocardiogram findings are consistent with diffuse cad and this testing could suggest minimal benefit from ptca and drive management toward a surgical strategy. the medical regimen for cad was optimized during this hospitalization with addition of aspirin, clopidogrel, and statin. the dose of statin was modified for concurrent cyclosporine use. he will follow up with dr. in cardiology clinic. 2) dysrrthymia: during his first night in the hospital the patient had a run of sustained ventricular tachycardia while resting comfortably and being monitored on telemetery. his blood pressure decreased from sbp's in the 140's to sbp's in the 110's, but mr remained completely asymptomatic during this episode. given concern this was possibly ischemia related vt, he was started on a lidocaine drip with resolution of his vt to nsr in a matter of one to two minutes. he was then transferred to the ccu for further management. in the ccu the patient was monitored on telemetry and stayed primarily in nsr with occasional incidents of nsvt that decreased in frequency over the course of his hospital stay. he was seen by ep, who thought given this was monomorphic vt with history of mi and hypo/akinetic apex this was most likely scar mediated vt. the plan was made to do a vt ablation at the same time of cardiac catheterization for revascularization. cardiac cathterization was canceled for the reasons described above but the electrophysiology service decided to proceed with the ablation and took the patient to the cath lab. unfortunately, during this procedure after receiving blood products and put in a supine position he became quite short of breath and hypoxic and was electively intubated for respiratory ditress. the vt ablation was unsuccessful and the patient was managed medically from that point forward. given the decreased incidence of nsvt over the course of his hospitalization the electrophysiology service did not recommend continuing anti-arrythmic therapy with anything but beta blocker. 3) acute systolic heart failure: at the time of presentation the patient had crackles to auscultation of his lung bases bilaterally and an oxygen requirement. given presumption of mi it was assumed he was in some degree of acute, decompensated heart failure and he had a brisk diuresis to a single dose of furosemide. early in the morning following admission the patient had an echocardiogram showing severe lv dysfunction with an ef of 15-20%. despite this, the patient had a stable respiratory status over the following day. he received one unit of blood with furosemide given at the same time and continued to have good oxygen saturations on a few liters of oxygen by nasal cannula. unfortunately, the following day after receiving two liters of blood in the cath lab and being put in a recumbent position the patient had an acutely worsened respiratory status and had to be intubated due to respiratory compromise. he also became hypotensive briefly and returned to the ccu from the cath lab on small doses of dopamine, which were weaned off over the following hours without recurrence of hypotension. while he was intubated he was diuresed approximately two liters, which required a furosemide drip after an inadequate response to bolus furosemide doses. after this diuresis he was s extubated without incident and continued to self diurese another liter without further diuretic therapy. he maintained approximate euvolemia after this without further need for diuretics. regarding chronic medical management of his heart failure, the patient was continued on his beta blocker. ace inhibitor therapy was considered but held due to the patient's acute renal failure. he was started on hydralazine and isosorbide as a substitute regimen for afterload reduction with plan to start ace inhibitor as an outpatient after renal function has improved to baseline. on discharge the patient has chronic heart failure given known reduced ef but was compensated without clinical signs of volume overload. 4) acute renal failure on chronic kidney disease: on presentation the patient's cr was elevated to 2.2 from baseline of 1.6. consideration was given to atn versus poor perfusion due to acute decompensated heart failure versus cyclosporine toxicity. cyclosporine level was found to be undetectable, but the first two diagnostic possibilities remained under consideration particularly as kidney function did not improve with initial heart failure management. thus, the nephrology service was consulted. they examined the urinary sediment and found no granular casts suggesting atn. this led to a presumptive diagnosis of prerenal failure due to poor systolic function and inadequate perfusion. as the patient's heart failure improved his cr improved as well and after peaking at 2.6 it had fallen back to 1.9 at discharge. 5) aplastic anemia: on presentation the patient's hematocrit was approximately 27, which is his baseline. over the next day, however, he fell to 25 and was given three units of blood in the hospital due to concern for anemia in the context of inadequate coronary perfusion. after these transfusions his hematocrit increased appropriately to 29 but then began to fall to around his baseline value of 26 at the time of discharge. the patient was also thrombocytopenic with relatively stable platelet counts of 70 to 100 during his hospitalization. his cyclosporine was held in the hospital due to concerns over his acute renal failure but restarted at the time of discharge. he will follow up with his regular hematologist, dr. . 6) diabetes mellitus: the patient was maintained on sliding scale insulin in the hospital with reasonable control of his blood glucose. 7) peripheral vascular disease: the patient is status post multiple peripheral vascular interventions with multiple bruits appreciated on physical exam. following his attempted percutaneous vt ablation he was found to have a cold, pulseless left foot that became mottled during the period there was a sheath in place. this exam improved with better color following sheath removal but pulses could still not be found with doppler. vascular surgery was consulted and chose to monitor given no signs of active ischemia and over the next day pulse returned and at discharge patient's foot at baseline with dopplerable but not palpable pulses. during this hospitalization mr. was started on aspirin, clopidogrel, and statin therapy for his cad, but these medical measures should also help manage his pvd. mr. was fed a cardiac, heart healthy diet in the hospital. he was kept on subcutaneous heparin for dvt prophylaxis. he was full code. medications on admission: folic acid 1 mg po daily metoprolol tartrate 50 mg po bid neooral 50 mg po qam and 25 mg po qpm nifedipine er 30 mg po daily discharge medications: 1. folic acid 1 mg tablet sig: one (1) tablet po daily (daily). 2. clopidogrel 75 mg tablet sig: one (1) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* 3. aspirin 325 mg tablet sig: one (1) tablet po daily (daily). 4. atorvastatin 10 mg tablet sig: one (1) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* 5. isosorbide dinitrate 20 mg tablet sig: three (3) tablet po tid (3 times a day). disp:*270 tablet(s)* refills:*2* 6. hydralazine 25 mg tablet sig: one (1) tablet po every eight (8) hours. disp:*90 tablet(s)* refills:*2* 7. metoprolol tartrate 50 mg tablet sig: 1.5 tablets po bid (2 times a day). disp:*90 tablet(s)* refills:*2* 8. neoral 25 mg capsule sig: three (3) capsule po once a day: please take two tablets each morning and one tablet each afternoon. . disp:*90 capsule(s)* refills:*2* discharge disposition: home with service facility: homecare discharge diagnosis: acute systolic congestive heart failure acute kidney injury on chronic kidney disease hypertension ventricular tachycardia aplastic anemia discharge condition: good, pain free, adequate o2 sats on room air discharge instructions: you had strain on your heart and an irregular heart rhythm called ventricular tachycardia. you had a procedure to try to prevent the ventricular tachycardia but had an acute episode of congestive heart failure during the procedure. you were intubated and on a ventilator to help you breathe. your kidneys were not working well because of your heart but now are getting better. your heart is weak and not pumping as well as it should. please weigh yourself every day in the morning before eating and call dr. is you have a weight gain of more than 3 pounds in 1 day or 6 pounds in 3 days. please also avoid salt in your diet, you should not eat more than 2000mg per day. . you need to have a stress test in 2 weeks and see dr. in 6 weeks. the cardiovascular clinic will call you about setting up this appointment with dr. . you also should have cardiac rehabilitation that will help your heart be as strong as it can be. . please stop smoking. information was given to you on admission regarding smoking cessation. followup instructions: provider: , md/ , md phone: date/time: 1:30. clinical center . cardiology: stress test: date/time: tuesday at 9:50am. building radiology department. no caffeine 12 hours before, no food or drink after midnight on . . provider: , md phone: date/time: at 11:20am. you should call the office after you are home and they have promised to get you an earlier appt. . please follow up with podiatry, call for an appointment md, procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours excision or destruction of other lesion or tissue of heart, endovascular approach cardiac mapping diagnoses: other primary cardiomyopathies subendocardial infarction, initial episode of care congestive heart failure, unspecified diabetes mellitus without mention of complication, type ii or unspecified type, not stated as uncontrolled acute kidney failure, unspecified hyposmolality and/or hyponatremia hypertensive chronic kidney disease, unspecified, with chronic kidney disease stage i through stage iv, or unspecified chronic kidney disease, unspecified paroxysmal ventricular tachycardia acute respiratory failure acute systolic heart failure aplastic anemia, unspecified 

Answer: The patient is high likely exposed to