(Circulation. 1996;94:3376-3381.)
© 1996 American Heart Association, Inc.
Articles |
Angina Pectoris and Progressive Fatigue in a 61-Year-Old Man
Correspondence to Stefan Schafer, MD, Medizinische Klinik und Poliklinik B, Abteilung fur Kardiologie, Pneumologie, und Angiologie, Heinrich-Heine-Universitat, Moorenstr 5, D-40225 Dusseldorf, Germany. E-mail sschaefe@uni-duesseldorf.de.
Key Words: Clinicopathological Conference • ischemia • amyloid • biopsy
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Case Presentation Stefan Schafer, MD |
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 Top Case Presentation Stefan... Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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History
A 61-year-old white male presented with exercise-induced chest discomfort and shortness of breath, occasionally associated with numbness in the left shoulder and elbow. Progressive weakness had forced him to reduce his physical activities in daily life. The patient's medical history included coronary artery disease without previous myocardial infarction. Six months earlier, coronary bypass surgery had been performed to the left anterior descending coronary artery (left internal thoracic artery) and its first diagonal branch (saphenous vein graft) at an outside institution with no complications. Thirteen years ago, he had undergone selective proximal vagotomy that had successfully terminated recurrent peptic ulcer disease. He had a history of mild systemic hypertension for
5 years that was effectively controlled by amlodipin (10 mg BID). The patient's other medication included acetylsalicylic acid (100 mg/d) and lovastatin (20 mg/d) for moderate hypercholesterolemia. He had a history of cigarette smoking of 25 pack-years until 3 years ago. There were no recent weight loss, no history of fever, and no night sweats. The patient attributed his symptoms to a progression of his coronary artery disease because he had experienced the same exercise-induced angina and dyspnea together with a feeling of physical weakness before coronary bypass surgery.
Physical Examination
On admission, the patient was alert and oriented. Physical examination was essentially normal, with the patient in no acute distress. His height was 175 cm; weight, 78 kg; pulse, constant at 74 bpm and regular; blood pressure, 120/70 mm Hg; respirations, 12 per minute; and axillary temperature, 36.8°C. There was no jugular venous distension or pitting edema. The lungs were clear to percussion and auscultation. Heart sounds were normal with no extra sounds or murmurs. The carotid and femoral pulses were normal without bruits; dorsalis pedis and pretibial pulses were 2+ bilaterally. There was no palpable cervical, axillary, or femoral lymphadenopathy. The abdomen was soft and nontender, with normal bowel sounds and no hepatosplenomegaly. Rectal examination was unremarkable, and a guaiac stool testing was negative. Neurological examination was normal; muscular strength was not reduced.
Initial Diagnostic Tests
Table 1
summarizes the laboratory findings on admission. In particular, slight anemia, hypercalcemia, and an elevated serum creatinine were noticed.
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The resting ECG showed a normal sinus rhythm, an axis of +80°, and nonspecific ST-segment and T-wave changes. The exercise ECG was highly abnormal (Fig 1), showing ST-segment depression in the precordial leads and T-wave inversion in leads II and III at a moderate level (75 W) of bicycle exercise.
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A chest radiograph was unremarkable except for slight elongation and sclerosis of the aorta. Heart size was at the upper normal limit. An ultrasound of the abdomen revealed no pathological findings.
Two-dimensional echocardiography showed a moderately enlarged left atrium (46 mm) and left ventricle (end diastolic diameter, 60 mm), with left ventricular wall thickness within normal limits. Left ventricular contractions appeared to be diffusely decreased to a moderate degree. Color Doppler analysis showed normal function of all heart valves.
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Clinical Discussion Stefan Schafer, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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This 61-year-old man with a known history of coronary artery disease and previous bypass surgery presented with exercise-induced chest discomfort, dyspnea, and progressive fatigue. The ECG indicated exercise-induced myocardial ischemia. In this setting, the obvious diagnosis is suspected progression of coronary artery disease or bypass graft dysfunction. Consequently, the next diagnostic step should be coronary angiography.
Certain features in this case, however, cannot be entirely explained by coronary artery disease alone, namely the patient's complaint of progressive physical weakness and the laboratory findings of anemia, hypercalcemia, and elevated serum creatinine.
Chronic fatigue and generalized weakness are rather nonspecific symptoms related to almost any systemic, infectious, or neoplastic disease. In addition, coronary artery disease may eventually lead to chronic fatigue, but this usually is the case when myocardial ischemia has led to congestive heart failure. Physical examination, however, did not reveal any signs of failure of the right or left side of the heart such as edema, jugular venous distention, or peripheral or pulmonary edema. An acute or chronic infection seemed unlikely because of the lack of fever, unremarkable physical examination, and normal white blood cell count. Tuberculosis must be considered, but the patient had no cough, and the chest radiograph showed no infiltration. A reduction in muscular strength is a known side effect of lipid-lowering drugs, in particular HMG–coenzyme A–reductase inhibitors. In large series, up to 5% of patients receiving lovastatin complained of muscular symptoms, including weakness or cramps.1 2 Therefore, lovastatin was discontinued.
The differential diagnosis of anemia commonly is based in part on the mean corpuscular volume. In this patient, normochromic normocytic anemia makes vitamin B12 or folic acid deficiency unlikely. The patient had a history of peptic ulcer disease. However, in the case of chronic bleeding, one would expect microcytic anemia. In addition, the normal iron and ferritin levels and the negative guaiac stool test make chronic bleeding an unlikely source of anemia in this patient. Although anemia of chronic disease typically is microcytic, a considerable portion of patients present without relevant changes in erythrocytic volume.3 Suppression of erythropoiesis such as in renal anemia or bone marrow infiltration also typically presents without specific changes of erythrocytic indexes. Another important feature in anemia is represented by serum iron and ferritin levels. In the present patient, these values were normal, which is typically the case in anemia because of bone marrow infiltration and in renal anemia. In contrast, anemia of chronic disease tends to present with decreased iron and increased ferritin levels.
Hypercalcemia goes along with a variety of disorders, particularly humoral, neoplastic, and renal. Parathormone levels were low, ruling out primary or secondary hyperparathyroidism. Sarcoidosis must be a consideration, but there were no abnormalities, such as enlarged hili or signs of lung fibrosis, on the chest radiograph, making this diagnosis more unlikely. Several malignancies typically go along with hypercalcemia, either by producing hormones that increase serum calcium levels or through osteolytic bone metastases, ie, cancer of the lung, prostate, or breast or multiple myeloma. Because of its high incidence, lung cancer must be strongly considered in this ex-smoker despite a normal chest radiograph and the lack of such clinical symptoms as cough or hemoptysis. Consequently, bronchoscopy might be performed as one of the next diagnostic procedures.
As suggested by the moderately elevated serum creatinine level and confirmed by the reduced creatinine clearance, renal insufficiency was present in this patient. Acute renal failure was unlikely because there was no history of recent trauma or surgery and daily urine production was normal. There was no hematuria or relevant albuminuria, ruling out acute nephritis and glomerular processes such as nephrotic syndrome. In light of the unremarkable ultrasound, some typical causes of chronic renal failure such as polycystic renal disease and chronic urinary obstruction can be excluded. Still, a wide range of diseases typically lead to chronic renal failure. Autoimmune disorders such as rapid progressive or poststreptococcal glomerulonephritis, Goodpasture's syndrome, or Wegener's granulomatosis usually lead to a relatively rapid deterioration of renal function within weeks or months. Hypertensive arteriolar nephrosclerosis, membranous glomerulonephritis, myeloma kidney, or amyloidosis typically go along with a more chronic course of renal failure.
With the patient's symptoms and laboratory findings discussed separately, it seems reasonable to look for potential causes for more than one of the patient's pathological findings, thereby identifying the more probable diagnoses from the large pool of possible explanations. Anemia and hypercalcemia may be related to renal failure, but renal anemia alone probably cannot explain the patient's weakness because the anemia was rather slight with a hemoglobin of 12 g/dL. Autoimmune disorders such as chronic polyarthritis or lupus erythematosus may go along with fatigue and anemia and may affect the kidneys. However, there were no accompanying clinical symptoms such as joint pain, erythema, or pleural effusion, and the patient's sex and age make these diagnoses unlikely. Nevertheless, subsequent specific laboratory testing was initiated that, however, did not confirm any autoimmune disorder. With regard to neoplasms, hematologic disorders such as multiple myeloma frequently lead to hypercalcemia, anemia, and renal failure. Therefore, further hematologic diagnostics were performed (see below).
Because of all these differential diagnoses, our first step was to perform coronary angiography to assess the degree of ischemic heart disease and to analyze left ventricular function.
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Cardiac Catheterization Matthias P. Heintzen, MD, and Bodo E. Strauer, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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Catheterization of the left side of the heart was performed by the conventional Judkins technique through the right femoral route. Coronary angiography revealed a moderate (50% to 70% eccentric) stenosis at the end of the proximal third of the left anterior descending coronary artery and a high-grade (99%) stenosis at the origin of its first diagonal branch. The circumflex and right coronary artery systems were free of relevant stenoses. The left internal thoracic bypass graft to the left anterior descending coronary artery and the saphenous vein graft to the first diagonal branch were patent. On injection of contrast media into the coronaries, however, a remarkable delay in contrast washout (coronary "slow-flow syndrome") was noticed. This phenomenon has been attributed to a hindrance of coronary flow at the microvascular level.4 The left ventricular angiogram showed a dilated left ventricle with a diffusely reduced ejection fraction.
Table 2 summarizes the catheterization data. The first coronary angiography (February 17, 1995) had been performed before the coronary bypass operation, 6 months before the present hospital stay. The second procedure was done on the second day of the present hospital stay (August 17, 1995). The third catheterization was performed 5 days later as an emergency procedure when an acute myocardial ischemic event was suspected (see "Clinical Course" below).
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In view of the patient's symptoms, abnormal exercise ECG, coronary slow-flow phenomenon, and diffusely reduced myocardial function, we suspected either coronary small-vessel disease or myocardial parenchymal disease and initiated further diagnostic procedures.
A myocardial single photon emission thallium scintigram (SPECT) confirmed exercise-induced myocardial ischemia, predominantly in the anterior wall and interventricular septum and also in the inferior left ventricular region (Fig 2).
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Hematologic Findings Ulrike Burkhard-Meier, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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In view of the anemia, hypercalcemia, and renal insufficiency, a concomitant hematologic disorder was suspected, and further laboratory and cytological workup was done. Serum protein electrophoresis revealed relative and absolute hypogammaglobulinemia (9.2% [3.5 g/dL]; norm, 10% to 15% [4.0 to 6.0 g/dL]); all other fractions were normal. No M gradient was present. Urine testing for Bence Jones proteinuria was positive. Subsequent immune electrophoresis revealed a monoclonal antibody light-chain–type
in serum and urine. Cytological analysis of a bone marrow aspirate showed a plasma cell infiltration of about 15%, with considerable plasma cell abnormalities such as enlarged nuclei, nuclear centralization, and double nuclear formation (Fig 3). Thus, the diagnosis of light-chain, or Bence Jones, myeloma was established.5
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In 5% to 20% of all plasma cell malignancies, only immunoglobulin light chains are secreted.5 6 Because typical features of multiple myeloma such as the characteristic M gradient in serum electrophoresis and a high plasma sedimentation rate are often absent and Bence Jones proteinuria usually is not detected by routine dipstick urinalysis, diagnosis of light-chain myeloma is often delayed. Light-chain myeloma is known to be associated with a high incidence of renal complications, caused by either precipitation of light chains in renal tubular cells or renal amyloidosis. Each of these two typical complications, alone or combined, may explain this patient's renal insufficiency.
Amyloidosis is a common feature of multiple myeloma. In large series, 60% of all patients with amyloidosis had multiple myeloma.7 In particular, amyloid deposition in the heart and kidneys is associated with a poor prognosis. Once congestive heart failure is present, median survival drops to 4 months.7
To obtain further prognostic information, quantitative analysis of protein excretion, determination of serum ß2-microglobulin, and radiographs of the skeleton in search for osteolytic lesions were recommended. Unfortunately, the rapid deterioration of the patient's overall status precluded these additional diagnostic tests. On the basis of hypercalcemia and renal insufficiency (serum creatinine >2.0 mg/dL), stage III B myeloma was determined, according to the classification of Durie and Salmon.8 The presence of Bence Jones proteinuria and renal dysfunction demands cytostatic therapy independent of the exact stage of the disease. Thus, intermittent courses of the alkylating agent melphalan (15 mg/m2 IV on day 1) plus prednisone (60 mg/m2 PO per day on days 1 through 4), repeated at 4- to 6-week intervals, were recommended.9 10
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Myocardial Biopsy R. Michael Klein, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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Because coronary angiography had ruled out relevant stenoses of the large coronary and bypass vessels in the presence of documented myocardial ischemia (ECG and thallium SPECT scintigraphy), coronary small-vessel disease was suspected. With left ventricular dilation and reduced ejection fraction, a generalized myocardial process such as myocarditis or dilated cardiomyopathy was another possibility. Cardiac amyloidosis, which in general is a rare finding, became more likely in view of the presence of light-chain multiple myeloma. Therefore, myocardial biopsies were taken from the right ventricular septum to gain more specific differential diagnostic information.
Histological examination (hematoxylin and eosin stain) revealed marked myocyte hypertrophy. There were foci of interstitial cells containing cells considered to be granulocytes, lymphocytes, and macrophages. In one specimen in which an arteriole was present, a homogeneous material was observed in the vessel wall that was identified as amyloid by Congo red staining. Interestingly, no interstitial amyloid was detected.
Immunoperoxidase staining revealed a mean of 4.0 T lymphocytes (CD3+) per high-power field (magnification x400, cells per 0.28 mm2) and demonstrated an average of 2.8 macrophages (MA 102) per high-power field. Additionally, excessive diffuse expression of human lymphocyte antigen classes I and II was found. In view of the coronary small-vessel disease and interstitial cell accumulation resulting from disseminated cell necroses, the positive immunohistochemical findings probably reflect a reactive postischemic immunologic process and do not necessarily suggest chronic myocarditis.
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Clinical Course |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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Over the next 5 days after admission, the patient's general condition deteriorated rapidly. Hemodynamic and respiratory failure developed, requiring intravenous catecholamines and oxygen up to 10 L/min through nasal cannula. On day 6, chest pain developed at rest. Another ECG showed ST-segment elevation in the inferior leads, and creatine kinase was increased to 172 U/L; creatine kinase–MB was significant at 24 U/L. In the presence of suspected acute myocardial infarction, another catheterization of the left side of the heart was performed, showing a slightly increased degree of narrowing in the left anterior descending coronary artery. Levocardiography demonstrated that left-side hemodynamics had dramatically worsened (see Table 2
). In a desperate effort to improve left ventricular function, a percutaneous transluminal coronary angioplasty to the left anterior descending coronary artery was performed. However, this maneuver did not bring significant hemodynamic improvement. Shortly thereafter, recurrent ventricular tachycardia occurred that required cardiopulmonary resuscitation. Stable hemodynamics could not be restituted, and the patient died in our intensive care unit on the sixth day of his hospital stay.
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Pathological Findings Cordula Schardt, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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At autopsy, severe cardiac hypertrophy was found (mass, 730 g). There was moderate atherosclerosis of the aorta, the large arteries, and the coronary arteries. Except for the first diagonal branch, which was almost obstructed by an atherosclerotic lesion, all coronary arteries and coronary bypass vessels were patent.
In contrast to that of the epicardial coronary arteries, histological examination of the heart revealed severe obstructive alterations of the intramural coronary arteries. Hematoxylin and eosin stain revealed large amounts of a homogeneous red material in the walls of virtually all intramural vessels of the left and right ventricle, leading to significant luminal narrowing or occlusion (Fig 4A). Congo red stain identified the occlusive material as amyloid (Fig 4B). Corresponding to the small-vessel-obstruction, disseminated fresh and, to some extent, older myocyte necroses at different stages of organization were found (Fig 4C). The fresh necrotic lesions presented with small infiltrates of granulocytes and lymphoid cells and a high number of plasma cells.
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Extracardiac abnormalities included an enlarged spleen (mass, 450 g) and pale, wax-like kidneys. Vascular amyloidosis was found in both organs and was demonstrated in the vessels of the lungs and liver. There was significant plasma cell infiltration of the bone marrow (40%), with a beginning displacement of the normal hematopoiesis. There was also diffuse plasma cell infiltration of the spleen and liver.
Other pathological findings included pulmonary emphysema and benign hyperplasia of the prostate. Also, there were residual signs of prolonged cardiopulmonary resuscitation such as petechial bleeding into the pericardium and the gastric mucosa.
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Conclusions Bodo E. Strauer, MD |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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This is a remarkable case of coronary small-vessel disease caused by cardiac amyloidosis. With this patient's coronary bypass graft 6 months earlier, the obvious primary diagnosis was progression of coronary artery disease. However, when coronary angiography had ruled out critical large-vessel stenosis and demonstrated left ventricular dysfunction, coronary small-vessel disease became more likely. Coronary insufficiency with a normal coronary angiogram is seen relatively often in clinical practice, amounting to 10% to 20% of all patients with exercise ECG abnormalities and positive response to nitroglycerin. In most of these patients, disturbances of the coronary microcirculation are present that may be related to metabolic, rheological, or microvascular abnormalities.11 Metabolic abnormalities include disturbances of oxygen diffusion and oxygen transport such as in methemoglobinemia or carbon monoxide intoxication. Rheological abnormalities can be assumed when a high blood or plasma viscosity is present such as in paraproteinemia, hyperlipoproteinemia, or erythrocytosis. Of the disorders at the microvascular level, hypertensive or diabetic microangiopathy are most common, but systemic collagen diseases and vasculitides (eg, lupus erythematosus, scleroderma, and immune complex vasculitis) also are frequent causes of coronary small-vessel disease.12 Coronary amyloidosis leading to profound exercise-induced myocardial ischemia such as in the present patient is certainly a rarity, and there have been only occasional reports of cardiac amyloidosis leading to coronary insufficiency.13 14 15 On the other hand, amyloidosis is a rather frequent feature of multiple myeloma. In multiple myeloma, the amyloid consists of immunoglobulin light chains and is referred to as primary amyloid or AL amyloid.16 The organs most likely to be involved are the kidneys and the heart.7 When cardiac amyloidosis is present, there is usually a considerable amount of interstitial amyloid, leading to congestive heart failure as the predominant symptom in most patients.17 18 In fact, endomyocardial biopsy reveals cardiac amyloidosis in
5% of patients with idiopathic heart failure.19 ECG findings include low voltage in the limb leads and conduction abnormalities.20 Further evaluation may be obtained with M-mode and Doppler echocardiography, which may show increased thickness of the interventricular septum and diastolic and systolic dysfunction.20 21 22 23 As this patient illustrates, however, a definite diagnosis cannot be established on the basis of these noninvasive techniques alone because of their limited sensitivity and specificity.20 In conclusion, in situations with unexplained myocardial ischemia and reduced cardiac function, a myocardial biopsy should be taken to obtain further differential diagnostic information. In the present patient, myocardial biopsy helped to establish the definite diagnosis of amyloidotic small-vessel disease. Unfortunately, the patient's overall state deteriorated progressively within a few days, and all diagnostic and therapeutic interventions failed to prevent the fatal outcome. Still, this case underlines the diagnostic importance of myocardial biopsy when ischemia with a normal or nearly normal coronary angiogram is present.
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Final Diagnosis |
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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Light-chain myeloma (IgG-type
) with coronary small-vessel amyloidosis.
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Footnotes |
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This Clinicopathological Conference was presented at the Heinrich-Heine-University Medical School, Dusseldorf, Germany, September 15, 1995.
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TopCase Presentation Stefan...Clinical Discussion Stefan...Cardiac Catheterization Matthias...Hematologic Findings Ulrike...Myocardial Biopsy R. Michael...Clinical CoursePathological Findings Cordula...Conclusions Bodo E. Strauer,...Final DiagnosisReferences |
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