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: aspirin / doxycycline hyclate attending: chief complaint: chest/lower abdominal quaking major surgical or invasive procedure: peripheral dopamine infusion drip iv history of present illness: pt is a 88 y/o cf with a pmh of chf with last ef >60%, as with valve area 0.7 cm2 (peak 84, mean 45), hypercholesterolemia, h/o atrial fibrillation off coumadin since admission for lower gi bleed, stated that last night she developed the acute onset of a "quaking" pressure across her lower chest/upper abdominal area. she states it was not a chest pain, just "discomfort". she states this would feel like a squeeze coming across her lower chest. it started around midnight. she did not sleep well, and when she got up this am, she stated it was still present. she assoc the squeeze with sob, no diaphoresis/n/v. no palpitations. no dizziness/lightheadedness. she states it resolved briefly this am after standing up, but then she lied back down and within minutes, the pressure was back. she states she has baseline sob, and sob with exertion, can walk steps and then is limited by dyspnea. no peripheral edema. no wt gain. no dietary changes, but reports poor po intake. occ pnd. stable 1 pillow orthopnea. . on arrival to , pt was noted to be in atrial fibrillation, vitals: bp: 221/66 p: 116 rr: 16 o2sat: 92-98% on 2l nc. she was afebrile at 96.9. she was given asa, 5mg iv lopressor, 25mg po lopressor x 2, 20iv lasix with no output, then 40iv lasix. 12 lead ekg demonstrated afib with rate 80s, new st segment depression v4-v6, although v4 more pronounced however ~0.5mm. biphasic t waves in precordial leads, present on prior ekg admission. she states she has been chest pressure free since she arrived to ed. no current sob. past medical history: 1. valvular ds: as (peak 84 mean 49), with valve area 0.7cm2. 2+mr, 2+ar, 1+ tr. 2. peptic ulcer disease with history of upper gi bleeding with egd showing gastric ulcer, per pt asa use, 3. h/o lgib on last admission , wherein she was found to likely have a left sided diverticular bleed. had colonoscopy at that time showing multiple severe non-bleeding diverticula with wide-mouth openings were seen in the sigmoid colon and descending colon. bleeding scan negative. coumadin stopped. 4. congestive heart failure with preserved ef 60%. 5. gout. 6. hypothyroidism. 7. depression 8. c-diff colitis in . 9. carpal tunnel syndrome. 10. afib - dx'd about 4 years ago, stopped coumadin on last admission 11. carotid stenosis 12. hernia repair around age 55 13. colon surgery for bowel obstruction in her 60s 14. h/o mult blood transfusions for ugib after ercp with sphincterotomy a few years ago. social history: father- died of mi at age 62, mother had chf, died at age , grandfather died of mi in his 60s. family history: pt is a former smoker, quit 40 years ago. only smoked 2 years ppd. no etoh. no ivda. lives in . physical exam: vs: t 96.9 bp: 167/39 p: 98 rr: 20 o2sat: 97% on 2l nc. gen: elderly female sitting in bed comfortably. pleasant, cooperative. aox3, somewhat hard of hearing b/l. heent: mmm, perrl, oropharynx clear. neck: jvp to 10cm. chest: crackles half way up lung fields bilaterally. cv: , +2/6 sem at rusb and apex, holosytolic murmur at apex abd: soft, nt, nd, nl active bowel sounds ext: trace peripheral edema bilaterally. 2+ dp pulses bilaterally. neuro: a&o x 3, moves all extremities. cn ii-xii intact pertinent results: tee: conclusions: no spontaneous echo contrast is seen in the body of the left atrium. no mass/thrombus is seen in the left atrium or left atrial appendage. mild spontaneous echo contrast is present in the left atrial appendage. the left atrial appendage emptying velocity is borderline depressed (0.2m/s). no spontaneous echo contrast or thrombus is seen in the body of the right atrium or the right atrial appendage. overall left ventricular systolic function is normal (lvef>55%). right ventricular systolic function is normal. there are complex (>4mm) atheroma in the aortic arch and descending thoracic aorta. the aortic valve leaflets are severely thickened/deformed with restricted mobility. the severity of the aortic stenosis could not be assessed with doppler. moderate (2+) aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. moderate (2+) mitral regurgitation is seen. the tricuspid valve leaflets are mildly thickened. impression: no atrial thrombus seen. . non contrast head ct findings: there is no evidence of acute intracranial hemorrhage or shift of normally midline structures. there is an old right insular cortical infarction. mild white matter hypoattenuation is consistent with microvascular ischemia and gliosis. no new areas of cortical attenuation abnormality are seen. again seen is a circular punctate calcified focus in the left temporal lobe, unchanged from prior study. there is fine heterogeneity of the skull attenuation, which is unchanged since the earlier ct. the paranasal sinuses clear. impression: no evidence of acute intracranial hemorrhage. no acute cortical territorial infarction is evident, but mr i is a more sensitive study to evaluate for acute infarction. . mri unable to be perfomed, pt's blood pressure too unstable. . ekg: atrial fibrillation at ~80bpm. nl axis. biphasic ts in v1-v6, st segment depressions in v4-v6, but most prominent in v4, and <0.5mm. compared with prior ekg dated , st dep in v4 more prominent. v5-6 no change. . cxr: single portable ap chest radiograph: again seen is an enlarged heart, stable as well as calcifications of the aortic knob. the mediastinal contours are unchanged. there is interstitial prominence as well as upper lobe pulmonary vascular redistribution. these findings are not significantly changed since the prior study. the previously seen pleural effusions have resolved. no pneumothoraces are evident. surrounding osseous structures demonstrate diffuse demineralization. impression: mild congestive heart failure. similar findings were also seen in . . last echo: the left atrium is markedly dilated. there is mild symmetric left ventricular hypertrophy with normal cavity size and systolic function (lvef>55%). regional left ventricular wall motion is normal. right ventricular chamber size and free wall motion are normal. the aortic valve leaflets are severely thickened/deformed. there is severe aortic valve stenosis. moderate (2+) aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. mild to moderate (+) mitral regurgitation is seen. there is moderate pulmonary artery systolic hypertension. there is a trivial/physiologic pericardial effusion. compared with the report of the prior study (images unavailable for review) of , the severity of aortic stenosis has increased (calculated valve area now severe) and the severity of aortic and mitral regurgitation are slightly reduced (may be related to lower blood pressure). the estimated pulmonary artery systolic pressure is also lower. . . prior imaging: colonoscopy: multiple severe non-bleeding diverticula with wide-mouth openings were seen in the sigmoid colon and descending colon. . - bleeding scan - no evidence of bleeding during the time of the study. . egd - gastric ulcer. , 10:10am blood wbc-8.0 rbc-4.14* hgb-11.9* hct-36.0 mcv-87 mch-28.8 mchc-33.1 rdw-17.1* plt ct-183, neuts-79.0* lymphs-14.0* monos-4.2 eos-1.8 baso-0.9 pt-11.8 ptt-28.3 inr(pt)-1.0 plt smr-normal plt ct-183 lplt-1+ glucose-114* urean-21* creat-1.0 na-139 k-4.8 cl-104 hco3-24 angap-16 glucose-127* urean-31* creat-1.5* na-137 k-5.1 cl-100 hco3-24 angap-18 glucose-116* urean-46* creat-2.2* na-135 k-4.6 cl-99 hco3-23 angap-18 glucose-108* urean-50* creat-2.4* na-136 k-4.9 cl-99 hco3-21* angap-21* glucose-117* urean-57* creat-2.9* na-137 k-4.8 cl-102 hco3-20* angap-20 glucose-123* urean-60* creat-3.2* na-136 k-5.3* cl-105 hco3-16* angap-20 glucose-132* urean-60* creat-3.3* na-135 k-7.2* cl-105 hco3-10* angap-27* ld(ldh)-827* ck(cpk)-41 alt-433* ast-372* ld(ldh)-393* alkphos-268* totbili-1.6* alt-515* ast-371* ld(ldh)-451* alkphos-332* totbili-1.2 ck-mb-notdone ctropnt-<0.01 probnp-6273* . brief hospital course: impression: 88 y/o woman with pmh significant for atrial fibrillation (was not on bb at ) off coumadin since for lgib, chf with preserved ef, likely diastolic component, severe aortic stenosis, 2+ mr, who presents hypertensive urgency, volume overload, in congestive heart failure, atrial fibrillation with rate ~115, and with lateral st depressions on ekg. unclear what precipitated the chf exacerbation, worsening aortic stenosis vs. atrial fibrillation with rvr, vs. ischemic event vs. severe hypertension, or some combination thereof. . #. atrial fibrillation: the cardiology team communicated with her outpatient cardiologist dr. nearly every day of this admission. dr. agreed with cardiology team that pt is poor anticoagulation candidate, given her prior history of large lower gi bleed in with coumadin being stopped then. dr. and dr. agreed that the benefit of getting the pt out of afib and into sinus with tee/cardioversion outweighs the risk of stroke, even though the pt would not be able to be on 4 weeks of anticoagulation. it was decided among all team members that if the tee demonstrated clot, no dc cardioversion would be performed. it was felt that a negative tee would minimize the risk somewhat of thrombus formation and subseuent embolus propagation. the pt was explained, in detail, the risks and benefits of tee/dc cardioversion and elected to proceed. on the day of , the day of tee/cardioversion, the pt demonstrated atn/shock liver hypoperfusion from low flow state, poor cardiac outflow secondary to multiple factors including end stage diastolic dysfunction, critical aortic stenosis, dehydration and poor po intake and acute oliguric renal failure. her mortality from these diagnoses alone was high, but it was decided that the pt's best chance to improve forward flow would be to get her out of atrial fibrillation, restoring her atrial kick and improving output. dr. and dr. discussed the options and risks at length, including the option for right heart cath vs. tee/dc cardioversion. it was decided among the team and dr. to proceed with tee/cardioversion. the tee fellow dr. and the ep fellow dr. obtained consent as well and explained risks and benefits. pt underwent tee showing no clot, and subsequently underwent dc cardioversion. the patient and daughter were informed of the risks of tee/dc cardioversion, including stroke, and it was discussed with pt and daughter that this risk is high in a patient not on anticoagulation (b/c of prior large lgib in when coumadin was stopped). since there was no evidence of clot on tee, the pt was cardioverted. post cardioversion, the pt was responsive, speaking to housestaff and rns. later in the evening of , the pt started having left sided weakness/paralysis, and altered mental status. night float intern was paged, and felt pt likely to have cva. ordered stat head ct, which was negative for bleed. consulted neurology and ordered mri, which was unable to be performed secondary to the pt's blood pressure being unstable. her systolic blood pressure drifted down to 30s systolic. of note, post dc cardioversion, she was hypotensive near 100-110s systolic. a trigger was called. the attending, dr. was called. the pt's daughter was telling the team not to place an arterial line or central venous line, given the pt had previously been dnr/dni on prior admissions, and these were her wishes. peripheral dopamine infusion was begun to bring up her blood pressure. she was transferred to the coronary care unit. in the ccu, the pt's vitals were monitored, with her blood pressure continuing to be low. neurology examined the patient, who by this time demonstrated no gag reflex, no corneal reflex, felt to have a basilar artery cerebrovascular accident either secondary to hypoperfusion or embolus. the pt's son, her health care proxy, was in , and it was decided to make the patient comfort measures only. she passed at 5:10am on . her daughter was present. her son declined the option to fly in from north . the pt was felt to have had a basilar artery infarct/cva secondary to hypoperfusion. also in the differential diagnosis is an embolus post dc cardioversion leading to basilar artery stroke. . #. coronaries: no prior cath, but mult risk factors for cad including age, hypercholesterolemia, htn, smoking history. with st depressions in lateral precordial leads. 3 sets of ce negative. we continued her beta blockers, statin and . the pt received asa in the ed, but was not given further asa given her h/o prior upper gi bleed and gastric ulcer aspirin use in the past. . #. pump: pt in heart failure with evid of vol overload on exam, elevated jvp to 10cm, bilateral crackles half way up lung fields. also with bnp 6000. unclear what precipitated the acute chf exacerbation: hypertensive, vs. worsening as vs. atrial fibrillation with rvr. her uop not responding to boluses and ivf hydration. urine lytes favoring prerenal azotemia. it was evident the pt had poor cardiac index and output as demonstrated by low flow state from severe diastolic dysfunction and severe aortic stenosis. the pt developed shock liver and acute tubular necrosis hypoperfusion. it was decided that she likely needed her atrial kick to increase her flow, and we proceeded with tee/dc cardioversion to correct this. see above for details of dc cardioversion. . #. electrical: see above under afib. . #. aortic stenosis, severe, with valve area 0.7cm2, peak 89, mean 45. we were cautious with diuresis. it was established that she is a poor surgical candidate for valvular repair this admission. . #. arf, oliguric- with cr to 2.9 today, up from cr 1.5 post 40mg iv lasix on admission. suspect oliguric arf prerenal azotemia poor forward flow (exacerbated by atrial fibrillation, severe as, dehydration, poor po intake). she did not respond to ivf continuous and ivf boluses. renal was consulted, and felt that there was no need for emergent hd, and recommended to address cardiac issues for low flow state, which was leading to hypoperfusion and atn. . # shock liver: pt's bp on admission was 220s/100, lowered over 48 hours to 100-120 systolic. pt with evid of atn, and shock liver by liver function tests, which are continuing to rise. pt has likely low flow state atrial fibrillation, severe as. see above under dc cardioversion. . #. htn: control with bb, . in the first 36 hours post admission, the pt's blood pressure dropped 100 systolic points through iv and po medications. it was thought that she may require higher pressures as she presented with bp 220/100, and within 48 hours, is 120s systolic. it was felt to contribute to her shock liver and atn. her post dc cardioversion course was complicated by severe hypotension requiring pressors. her cva was thought possibly hypoperfusion/low bp vs. embolic. . #. mdd- we continued her outpt prozac, social work consult for coping, encouraged po intake. she was very depressed, and told her daughter and intern that she she "was in the process of dying." . #. hypothyroidism: we continued outpt synthroid. . #. hypercholesterolemia- we continued her outpt lipitor. . #. fen: cardiac/heart healthy diet. replete lytes for k>4, mg>2. ivf prn. . #. dnr/dni/cmo. . #. all communication was with with patient and daughter . cell phone: . and health care proxy, her son, number in chart. medications on admission: 1. atorvastatin 10 mg tablet sig: one (1) tablet po daily (daily). 2. oxazepam 10 mg capsule sig: one (1) capsule po hs (at bedtime) as needed. 3. levothyroxine 88 mcg tablet sig: one (1) tablet po daily (daily). 4. pantoprazole 40 mg tablet, delayed release (e.c.) sig: one (1) tablet, delayed release (e.c.) po q24h (every 24 hours). 5. fluoxetine 20 mg capsule sig: one (1) capsule po daily (daily). 6. amiodarone 200 mg tablet sig: one (1) tablet po daily (daily). 7. ipratropium bromide 0.02 % solution sig: one (1) nebulizer inhalation q6h (every 6 hours) as needed for dyspnea. 8. furosemide 80 mg tablet sig: one (1) tablet po once a day. 9. losartan 50 mg tablet sig: one (1) tablet po once a day. disp:*30 tablet(s)* refills:*2* 10. allopurinol 300 mg tablet sig: one (1) tablet po once a day. 11. colace 100 mg capsule sig: one (1) capsule po twice a day. disp:*60 capsule(s)* refills:*2* 12. magnesium oxide 400 mg tablet sig: one (1) tablet po once a day. discharge medications: not applicable discharge disposition: expired discharge diagnosis: 1. basilar cerebrovascular accident secondary to hypoperfusion versus embolus 2. atrial fibrillation 3. severe diastolic congestive heart failure 4. severe aortic stenosis 5. hypertensive urgency 6. oliguric acute renal failure 7. shock liver secondary to hypoperfusion 8. hypercholesterolemia 9. major depressive disorder 10. urinary tract infection discharge condition: expired discharge instructions: not applicable followup instructions: not applicable md, procedure: diagnostic ultrasound of heart other electric countershock of heart infusion of vasopressor agent diagnoses: pure hypercholesterolemia acute kidney failure with lesion of tubular necrosis urinary tract infection, site not specified acute and subacute necrosis of liver unspecified acquired hypothyroidism gout, unspecified atrial fibrillation mitral valve insufficiency and aortic valve insufficiency occlusion and stenosis of carotid artery without mention of cerebral infarction rheumatic heart failure (congestive) major depressive affective disorder, single episode, unspecified dehydration cerebral artery occlusion, unspecified with cerebral infarction diseases of tricuspid valve diverticulosis of colon (without mention of hemorrhage) 

Answer: The patient is high likely exposed to