Spontaneous calcified cerebral emboli (SCCE) secondary to aortic valve calcification are a rare and underreported cause of acute ischaemic stroke. Only five cases of SCCE secondary to bicuspid aortic valve calcification have been reported in the literature. This review includes a unique case example of acute ischaemic stroke secondary to SCCE, as the first manifestation of a calcified bicuspid aortic valve. This is the first clinical case of calcified cerebral emboli (CCE) associated with borderzone infarction ('cortical ribbon sign'). Whilst previously assumed that most CCE are secondary to iatrogenic causes, recent literature suggests the majority of CCE are spontaneous and clinically silent. Despite CT imaging widely considered the 'gold standard' for diagnosis, CCE are frequently misdiagnosed and missed entirely. Misdiagnosis of CCE may have catastrophic consequences due to the high risk of recurrence and missed opportunity to prevent neurological disability and death. This review presents a revised CCE diagnostic criteria, using evidence that has emerged over the last decade to create both Compulsory (Major) and Supporting (Minor) criteria. Current CCE management is not evidence based and remains largely speculative. SCCE may be the first manifestation of cardiac or vascular disease and diagnosis should trigger aggressive treatment of emboligenic sources. Future epidemiological studies, analysing symptomatic and asymptomatic SCCE patients, would be beneficial in providing accurate quantification of disease burden. Other future research directions include exploring intracranial stenting for CCE revascularisation and cerebral intravascular lithotripsy.

Embolic stroke of undetermined source is a challenging clinical entity. While less common than atrial fibrillation and endocarditis, many noninfective heart valve lesions have been associated with stroke and may be considered as culprits for cerebral infarcts when other more common causes are excluded. This review discusses the epidemiology, pathophysiology, and management of noninfective valvular diseases that are commonly associated with stroke.

Calcific debris from degenerating aortic and mitral valves may embolize to the cerebral vasculature causing small- or large-vessel ischemia. Thrombus which may be adherent to calcified valvular structures or left-sided cardiac tumors may also embolize resulting in stroke. Tumors themselves, most commonly myxomas and papillary fibroelastomas, may fragment and travel to the cerebral vasculature. Despite this broad differential, many types of valve diseases are highly comorbid with atrial fibrillation and vascular atheromatous disease. Thus, a high index of suspicion for more common causes of stroke is needed, especially given that treatment for valvular lesions typically involves cardiac surgery whereas secondary prevention of stroke due to occult atrial fibrillation is readily accomplished with anticoagulation.

Background Description of cerebral and retinal infarction in patients with bicuspid aortic valve (BAV) is limited to case reports. We aimed to characterize cerebral and retinal infarction and examine outcomes in patients with BAV. Methods and Results Consecutive patients from 1975 to 2015 with BAV (n=5401) were retrospectively identified from the institutional database; those with confirmed cerebral or retinal infarction were analyzed. Infarction occurring after aortic valve replacement was not included. Patients were grouped according to infarction pathogenesis: embolism from a degenerative calcific BAV (BAVi); non-BAV, large artery atherosclerotic or lacunar infarction (LAi); and non-BAV, non-large artery embolic infarction (nLAi). There were 83/5401 (1.5%) patients, mean age 54±12 years and 28% female, with confirmed cerebral or retinal infarction (LAi 23/83 [28%]; nLAi 30/83 [36%]; BAVi 26/83 [31%]; other 4/83 [5%]). Infarction was embolic in 72/83 (87%), and 35/72 (49%) were cardioembolic. CHA₂DS₂-VASc score was 1.4±1.2 in BAVi (P=0.188 versus nLAi) and 2.3±1.2 in LAi (P=0.005). Recurrent infarction occurred in 41% overall (50% BAVi, P=0.164 and 0.803 versus LAi and nLAi). BAVi was more commonly retinal (39% BAVi versus 13% LAi, P=0.044 versus 0% nLAi, P=0.002). Patients with BAVi and LAi were more likely to have moderate-to-severe aortic stenosis and undergo aortic valve replacement compared with patients with nLAi. Conclusions Cardioembolism, often from degenerative calcification of the aortic valve, is a predominant cause of cerebral and retinal infarction in patients with BAV and is frequently recurrent. Cerebral and retinal infarction should be regarded as a complication of BAV.

The detection of cardiac valvular calcification on routine imaging may provide an opportunity to identify individuals at increased risk for peripheral artery disease (PAD). We investigated the associations of aortic valvular calcification (AVC) and mitral annular calcification (MAC) with risk of developing clinical PAD or a low ankle-brachial index (ABI).

AVC and MAC were measured on cardiac computed tomography in 6778 Multi-Ethnic Study of Atherosclerosis participants without baseline PAD between 2000 and 2002. Clinical PAD was ascertained through 2015. Incident low ABI, defined as ABI <0.9 and decline of ≥0.15, was assessed among 5762 individuals who had an ABI >0.9 at baseline and at least one follow-up ABI measurement 3-10 years later. Adjusted Cox proportional hazards and Poisson regression modelling were used to determine the association of valvular calcification with clinical PAD and low ABI, respectively. There were 117 clinical PAD and 198 low ABI events that occurred over a median follow-up of 14 years and 9.2 years, respectively. The presence of MAC was associated with an increased risk of clinical PAD [hazard ratio 1.79; 95% confidence interval (CI) 1.04-3.05] but not a low ABI (rate ratio 1.28; 95% CI 0.75-2.19). No significant associations were noted for the presence of AVC and risk of either clinical PAD.

MAC is associated with an increased risk of developing clinical PAD. Future studies are needed to corroborate our findings and better understand whether MAC holds any predictive value as a risk marker for PAD.

Valvular heart disease (VHD) is frequently associated with neurologic complications. Cerebral embolism is the most common, since thrombus formation results from the abnormalities in the valvular surfaces and the anatomic and physiologic changes associated with valve dysfunction, including atrial or ventricular enlargement, intracardiac thrombi, and cardiac dysrhythmias. Prosthetic heart valves, particularly mechanical valves, are very thrombogenic, which explains the high risk of thromboembolism and the need for long-term anticoagulation. Transcatheter aortic valve replacement (TAVR) has emerged as a nonoperative alternative to surgical aortic valve replacement for patients with intermediate or high surgical risk, and the procedure also has a risk of cerebral ischemia. In addition, anticoagulation, the mainstay of treatment to prevent cerebral embolism, has known potential for hemorrhagic complications. The emergence of new oral anticoagulants with similar effectiveness to warfarin and a better safety profile has facilitated the management of patients with atrial fibrillation. However, their application in patients with mechanical heart valves is still evolving. The prevention and management of these complications requires an understanding of their natural history to balance the risks posed by valvular heart disease, as well as the risks and benefits associated with the treatment.

Background and Purpose- Aortic valve stenosis may lead to atrial and ventricular remodeling, predisposes to atrial fibrillation, and may also be an independent risk factor of ischemic stroke. However, information on stroke rates among persons with aortic valve stenosis are sparse. We aimed to determine the incidence rates and relative risks of ischemic stroke in individuals with diagnosed aortic valve stenosis compared with age- and sex-matched controls. Methods- All patients with incident aortic valve stenosis aged >18 years (n=79 310) and age- and sex-matched controls were identified using the Danish nationwide registries (1997-2017). Incidence rates per 1000 person-years (PY) and multivariable adjusted hazard ratios with 95% CIs were reported. Results- In total, 873 373 individuals (median age 77 years, 51.5% men, 9.1% with aortic valve stenosis) were included. Ischemic stroke occurred in 70 205 (8.0%) individuals during 4 880 862 PY of follow-up. Incidence rates of ischemic stroke were 13.3/1000 PY among the controls compared with 30.4/1000 PY in patients with aortic valve stenosis, corresponding to a hazard ratio of 1.31 (95% CI, 1.28-1.34). In all age-groups, the incidence rates and relative risks were significantly increased in patients with aortic valve stenosis compared with controls, but the relative risk was greater for younger individuals (eg, age group, 18-45 years: hazard ratio, 5.94 [95% CI, 4.10-8.36]). In patients with aortic valve stenosis above 65 years of age, the risk of ischemic stroke was markedly lower after aortic valve replacement (30.3 versus 19.6/1000 PY before and after valve replacement). Among people with atrial fibrillation the incidence rate of ischemic stroke was 1.5 times higher when aortic valve stenosis was present (33.0/1000 PY versus 49.9/1000 PY). Conclusions- People with aortic valve stenosis have a significantly increased risk of ischemic stroke compared with age- and sex-matched controls. Future studies are warranted to explore whether antithrombotic therapy may be beneficial in some individuals.

Calcified cerebral emboli (CCE) are rarely responsible for large vessel occlusion (LVO) in acute anterior stroke, and therefore therapeutic experience is scarce. We sought to expand current knowledge upon therapeutic options with three new cases and a review of current literature.

Systematic search of patients with acute anterior stroke due to LVO in one comprehensive stroke center throughout a 4 year period. Literature search for reported cases of CCE.

In total, 21 cases (19 found in literature and 3 from our institution) are reported with a median age of 72 years (interquartile range [IQR] 63-80). Eleven patients were treated acutely, 4 of them with endovascular thrombectomy (EVT). Middle cerebral artery (MCA) M1 was the most affected segment and large artery atherosclerosis (LAA) and cardioembolism (CE) was causative in 41% of cases. EVT was significantly superior to intravenous recombinant tissue plasminogen activator (rtPA) at p = .048 (Fisher's exact test, chi square 6.7).

Given the small sample reported in literature and no reported randomised studies, definitive recommendations could not be reached. However, considering thrombus composition, thrombolysis is most probably not sufficient and priority should be given to EVT.

The association of severe calcific aortic stenosis with clinically significant stroke has not been well established. This case vividly describes the relationship with clinical and pathological (gross and microscopic) findings in a 62-year-old man with a severely calcified bicuspid aortic valve. Eleven months prior to aortic valve surgery, the patient had stigmata of cerebral embolic events in the absence of any other embolic source. During the aortic valve replacement surgery for aortic stenosis, he was found to have a large atheroma on the aortic valve cusp with a crater containing friable debris in its center. These findings support the potential for embolic stroke in patients with severe calcific aortic stenosis. We recommend that the aortic valve be considered as an embolic source in patients with an otherwise cryptogenic cerebrovascular accident.

Valvular heart disease (VHD) is frequently associated with neurologic complications; cerebral embolism is the most common of these since thrombus formation results from the abnormalities in the valvular surfaces or from the anatomic and physiologic changes associated with valve dysfunction, such as atrial or ventricular enlargement, intracardiac thrombi, and cardiac dysrhythmias. Prosthetic heart valves, particularly mechanical valves, are very thrombogenic, which explains the high risk of thromboembolism and the need for anticoagulation for the prevention of embolism. Infective endocarditis is a disease process with protean manifestations that include not only cerebral embolism but also intracranial hemorrhage, mycotic aneurysms, and systemic manifestations such as fever and encephalopathy. Other neurologic complications include nonbacterial thrombotic endocarditis, a process associated with systemic diseases such as cancer and systemic lupus erythematosus. For many of these conditions, anticoagulation is the mainstay of treatment to prevent cerebral embolism, therefore it is the potential complications of anticoagulation that can explain other neurologic complications in patients with VHD. The prevention and management of these complications requires an understanding of their natural history in order to balance the risks posed by valvular disease itself against the risks and benefits associated with treatment.

The objective of this study was to investigate the associations of mitral annular calcification, aortic annular calcification, and aortic valve sclerosis with covert magnetic resonance imaging (MRI)-defined brain infarcts.

Clinically silent brain infarcts defined by MRI are associated with increased risk for cognitive decline, dementia, and future overt stroke. Left-sided cardiac valvular and annular calcifications are suspected as risk factors for clinical ischemic stroke.

A total of 2,680 CHS (Cardiovascular Health Study) participants without clinical histories of stroke or transient ischemic attack underwent brain MRI in 1992 and 1993, 1 to 2 years before echocardiographic exams (1994 to 1995).

The mean age of the participants was 74.5 ± 4.8 years, and 39.3% were men. The presence of any annular or valvular calcification (mitral annular calcification, aortic annular calcification, or aortic valve sclerosis), mitral annular calcification alone, or aortic annular calcification alone was significantly associated with a higher prevalence of covert brain infarcts in unadjusted analyses (p < 0.01 for all). In models adjusted for age, sex, race, body mass index, physical activity, creatinine, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, smoking, diabetes, coronary heart disease, and congestive heart failure, the presence of any annular or valve calcification remained associated with covert brain infarcts (risk ratio: 1.24; 95% confidence interval: 1.05 to 1.47). The degree of annular or valvular calcification severity showed a direct relation with the presence of covert MRI findings.

Left-sided cardiac annular and valvular calcifications are associated with covert MRI-defined brain infarcts. Further study is warranted to identify mechanisms and determine whether intervening in the progression of annular and valvular calcification could reduce the incidence of covert brain infarcts as well as the associated risk for cognitive impairment and future stroke.

Calcific cerebral emboli are a known complication of aortic stenosis. Most of these emboli are related to traumatic disruption, via cardiac catheterization, valvotomy, or valve replacement. Spontaneous calcific cerebral emboli are extremely rare and are typically associated with heavily calcified bicuspid aortic valves, especially when they occur in young adults. The authors report a case of a spontaneous calcific embolic infarction in a 40-year-old man with a trileaflet aortic valve.

To describe the association between calcific retinal embolism (CRE) and cardiac valve stenosis.

Retrospective chart review of patients with clinical criteria for CRE.

24 patients with CRE who underwent two dimensional echocardiography between 1976 and 1998.

Nine patients (38%) had calcific valve stenosis, which was haemodynamically severe in five patients (four aortic and one mitral), four of whom had no cardiac symptoms. Six patients underwent surgical intervention (aortic valve replacement in three patients, mitral and aortic valve replacement in one patient, removal of calcific cardiac pseudotumour in one patient, and carotid endarterectomy in one patient).

CRE may be the presenting feature of otherwise asymptomatic, clinically important underlying cardiovascular disease and, in particular, haemodynamically severe calcific valve stenosis.

This chapter about antithrombotic therapy in native and prosthetic valvular heart disease is part of the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following: For patients with rheumatic mitral valve disease and atrial fibrillation (AF), or a history of previous systemic embolism, we recommend long-term oral anticoagulant (OAC) therapy (target international normalized ratio [INR], 2.5; range, 2.0 to 3.0) [Grade 1C+]. For patients with rheumatic mitral valve disease with AF or a history of systemic embolism who suffer systemic embolism while receiving OACs at a therapeutic INR, we recommend adding aspirin, 75 to 100 mg/d (Grade 1C). For those patients unable to take aspirin, we recommend adding dipyridamole, 400 mg/d, or clopidogrel (Grade 1C). In people with mitral valve prolapse (MVP) without history of systemic embolism, unexplained transient ischemic attacks (TIAs), or AF, we recommended against any antithrombotic therapy (Grade 1C). In patients with MVP and documented but unexplained TIAs, we recommend long-term aspirin therapy, 50 to 162 mg/d (Grade 1A). For all patients with mechanical prosthetic heart valves, we recommend vitamin K antagonists (Grade 1C+). For patients with a St. Jude Medical (St. Paul, MN) bileaflet valve in the aortic position, we recommend a target INR of 2.5 (range, 2.0 to 3.0) [Grade 1A]. For patients with tilting disk valves and bileaflet mechanical valves in the mitral position, we recommend a target INR of 3.0 (range, 2.5 to 3.5) [Grade 1C+]. For patients with caged ball or caged disk valves, we suggest a target INR of 3.0 (range, 2.5 to 3.5) in combination with aspirin, 75 to 100 mg/d (Grade 2A). For patients with bioprosthetic valves, we recommend vitamin K antagonists with a target INR of 2.5 (range, 2.0 to 3.0) for the first 3 months after valve insertion in the mitral position (Grade 1C+) and in the aortic position (Grade 2C). For patients with bioprosthetic valves who are in sinus rhythm and do not have AF, we recommend long-term (> 3 months) therapy with aspirin, 75 to 100 mg/d (Grade 1C+).

The clinical relevance of cardiac embolism a potential cause of stroke is progressively increasing, mainly due to the recent progress in diagnostic imaging. In the present paper, we update and review the state of the art of the different etiologies currently accepted of a cardiac source of stroke. Furthermore, we review the clinical role of different image techniques, emphasizing the doubts and realities of each particular approximation.

We report a case of a mobile calcific mass on the aortic valve that prolapsed into the left main coronary artery of a 51-year-old man. This case and a review of the literature suggest that calcific embolization to coronary arteries is a rare but possibly underrecognized complication of calcified degenerative or bicuspid aortic valves. This potentially catastrophic complication of calcified aortic valves needs to be suspected and recognized in clinical practice.

The use of antithrombotic agents to prevent thromboembolic events in patients with valvular heart disease is common. Recent studies using improved diagnostic techniques have allowed better elucidation of valvular abnormalities and re-evaluated the incidence and risk of thromboembolism. We review the recent literature examining the risk of thromboembolic events in various valvular abnormalities, and the use of different antithrombotic agents in the prevention of thromboembolic events. We also review the current recommended practice in both native valve abnormalities and prosthetic heart valves.

Exercise stress ECG testing is not generally recommended in patients with severe aortic stenosis. Analysis of the utility of exercise testing, both with and without the use of myocardial thallium-201 scintigraphy for the diagnosis of coronary artery disease (CAD), yielded low specificity. A noninvasive, safe, and accurate diagnostic modality to ascertain the presence of CAD is not available to date for patients with severe aortic stenosis. The aim of this study was to assess the safety and diagnostic accuracy of adenosine stress echocardiography (A-Stress-Echo) and of adenosine stress myocardial perfusion scintigraphy (A-SPECT), for the detection of CAD in patients with severe aortic stenosis. The study included 50 patients with severe aortic stenosis (maximal instantaneous aortic valve gradient >80 mmHg, range 81 to 144 mmHg, and aortic valve area <0.75 cm2). All patients were submitted to A-Stress-Echo, after a 6-minute infusion of adenosine (140 microg/kg body weight/min), and then (>3 days later) A-SPECT with the same dosage of adenosine as above. Coronary angiography was performed in all patients. No major complications were observed. The unpleasant symptoms were brief and did not necessitate cessation of the test. Both modalities showed the same sensitivity (85% for A-SPECT and 85% for A-Stress-Echo) angiographically diagnosed CAD while A-Stress-Echo yielded much higher specificity (96.7% vs 76.7%). Concordance of the two methods was found in 40 cases and the specificity for those patients was 100%. A-Stress-Echo and A-SPECT, either separately or in combination, constitute excellent and safe noninvasive diagnostic methods in detecting CAD in patients with severe aortic stenosis.

This is the first documented case of a patient suffering from embolic occlusion of the left brachial artery caused by a large embolus growing on a lesion of a stenosed calcified aortic valve. Supported by their own additional observations the authors suggest that severe calcified aortic valve stenosis should be considered as an indication for anticoagulation in the period before surgical valve replacement.

Patients with heart valve disease have rheologic abnormalities that are more pronounced in double valve disease than in mitral or aortic valve disease; after valve replacement surgery, the degree of rheologic abnormality is more pronounced in patients with mechanical and biological prostheses than in those with homografts and pulmonary autografts. Rheologic abnormalities seen in these patients might be related to the different incidences of thromboembolism in the presence of various valve defects and various types of prostheses.

Nonrheumatic atrial fibrillation (AF) frequently coexists with other risk factors for cerebral ischemia. This study was originally designed to determine which combinations of clinical and echocardiographic abnormalities were most closely associated with the risk of cerebral ischemic events. Patients with cerebral ischemic events (n = 214) and community-based control subjects (n = 201) underwent transesophageal echocardiography and carotid artery imaging. Adjusted odds ratios (ORs) were determined using multiple logistic regression analysis. Independent risk factors for cerebral ischemia included diabetes, carotid stenosis, aortic sclerosis, left ventricular dysfunction, left ventricular hypertrophy, left atrial (LA) spontaneous contrast, and proximal aortic atheroma. Nonrheumatic AF in combination with LA spontaneous contrast and LA enlargement showed a strong association with cerebral ischemic events (OR 33.7 [95% confidence interval 4.53 to 251]). In subjects with sinus rhythm or nonrheumatic AF, LA enlargement was not associated with an increased risk of cerebral ischemic events in the absence of LA spontaneous contrast. However, only 2 patients and 1 control subject had nonrheumatic AF without LA spontaneous contrast or LA enlargement. Therefore, study of a larger number of subjects is required to address the issue of whether nonrheumatic AF itself carries increased risk. The combination of nonrheumatic AF with LA spontaneous contrast is a potent risk factor for cerebral ischemia. Ascertaining the risk factor in nonrheumatic AF requires adequate examination for underlying cardiac, aortic, and carotid vascular disease. Transesophageal echocardiography may contribute to this assessment.

In a population sample of 501 persons aged 75 to 86 years, Doppler echocardiography uncovered moderate or severe aortic valve stenosis in 8.8% of women and 3.6% of men. Severe aortic valve stenosis predicted a four-fold-age- and sex-adjusted risk of death within 4 years of diagnosis, and mortality tended to be increased also with moderate lesions; mild aortic valve stenosis had a favorable outcome.

Retinal artery embolization is an unusual but serious complication of calcific aortic stenosis. However, it is rare for retinal embolization to be the presenting feature of aortic stenosis. This report describes a young patient who presented with an acute retinal artery occlusion secondary to calcific aortic valve disease, and discusses the rationale for early surgical intervention.

A 77-year-old man underwent coronary artery angiography quite well. However, several attempts were required to pass the pigtail catheter across a calcified stenotic aortic valve. On return to the floor, motor aphasia and right hemiparesis developed and improved steadily within a few days. Computed tomography (CT) of the head revealed a calcific density in the left middle cerebral artery. The authors believe the calcific plaque originated from the calcified aorta and aortic valve. The patient was discharged within 48 hours with minimal neurological signs. Spontaneous calcified emboli to cranial vessels from calcific aortic stenosis or other sources are rare. CT detection of a calcific plaque in a cranial vessel following coronary vessel catheterization is well documented in this patient.

Calcific embolization from aortic stenosis may be more frequent than commonly appreciated. Most calcific emboli are clinically silent, although transient ischemic attacks, cerebral infarcts, blindness (from central retinal artery occlusions), and myocardial infarctions have been reported. We describe a patient with calcific bicuspid aortic stenosis who presented with transient ischemic attacks and angina secondary to a calcific embolus to the second circumflex marginal coronary artery. The calcific embolus was retrieved during aortic valve replacement surgery. A review of the literature suggests that calcific embolization from calcific aortic stenosis may occur more commonly in patients with bicuspid valves.

The case described is a death due to embolization of calcium debris from a bioprosthesis, dislodged at cardiac catheterization. As more bioprosthetic valves are implanted, and more of them fail long-term with calcification, such complications of the invasive study of these valves may be expected.

We report a patient with moderate aortic stenosis who had two episodes of calcium embolus to the left popliteal artery within ten months. This case suggests that calcium emboli can be recurrent and that major calcium emboli should warrant consideration of valve replacement, even in patients with mild aortic stenosis.

The long term performance characteristics of the 2400 and 1260 series of Starr-Edwards aortic prostheses were investigated by a follow up study of clinical outcome of 327 patients discharged from hospital with isolated aortic valve replacement. Follow up lasted for up to 10 years and was based on 1616 patient-years. The 2400 series cloth covered tracked valve was implanted in 182 patients from 1974 to 1980 and the 1260 series bare strut silastic ball valve was inserted in 145 patients from 1979 to 1983. Total 10 year mortality and valve related morbidity were low and no cases of mechanical valve failure were recorded. There were no significant actuarial differences in mortality or valve related morbidity between the 2400 and 1260 valves. Starr-Edwards models 2400 and 1260 aortic valve prostheses showed excellent durability without any mechanical failures over a 10 year period. The long term outcome of isolated aortic valve replacement with these models is associated with a low frequency of valve related complications.

Indications and the type of antithrombotic therapy for the prevention of thromboembolism in patients with valvular heart disease, mechanical prosthetic heart valves and bioprosthetic heart valves are discussed. The evidence for these clinical recommendations is described and graded into five levels. The indications for anticoagulation in patients with valvular heart disease are chronic or paroxysmal atrial fibrillation, sinus rhythm with a very large left atrium, severe left ventricular dysfunction or presence of heart failure or a history of previous thromboembolism. Anticoagulant therapy is administered to prolong the prothrombin time to 1.5 to 2.0 times control, using rabbit brain thromboplastin (standardized international normalized ratio = 3.0 to 4.5). Risk factors for thromboembolism in patients with prosthetic heart valves are discussed. Because intracardiac thrombus formation may start during and continues early after operation, restarting heparin therapy 6 hours after operation and continuing it for the duration of the hospitalization is advised. For mechanical prosthetic heart valves, oral anticoagulation as outlined plus dipyridamole is advised indefinitely. Platelet inhibitor therapy alone is insufficient. For bioprosthetic heart valves, heparin is followed by oral anticoagulation as outlined for 3 months after mitral or aortic valve replacement and indefinitely after mitral valve replacement if there is atrial fibrillation or a very large left atrium; aspirin may be recommended indefinitely after aortic valve replacement. Antithrombotic therapy is also considered for four special situations: noncardiac surgery, prosthetic valve endocarditis, anticoagulation after a thromboembolic event, and antithrombotic therapy during pregnancy.

The association of heart disease and cerebral ischemic attacks, and the usefulness of echocardiography in detecting heart disease and possible embolic source, were studied in 194 patients with transitory cerebral ischemic attack or stroke. The study revealed 95 patients with heart disease, and 63 of them had positive echocardiographic findings. All together, 35 patients had heart disease as a probable source for systemic embolism. An undetected cardiac disorder, not found by clinical examination or electrocardiography, was detected in 25 patients. The cardiac disorder found by echocardiography only, was most frequently aortic and mitral valve disease. Thus, echocardiography is an useful tool in detecting heart disease in these patients.

A massive embolus of the central retinal artery occurred during cardiac catheterization and selective coronary angiography. Anterior chamber paracentesis and coughing resulted in restoration of retinal blood flow and vision within two hours. In two other cases retinal arteriolar embolization was observed in patients who had minimal or no ocular symptoms after cardiac catheterization.