N-terminal pro-B-type natriuretic peptide and B-type natriuretic peptide for identifying coronary artery disease and left ventricular hypertrophy in ambulatory chronic kidney disease patients.

Elevated natriuretic peptide levels are common in patients with chronic kidney disease (CKD), as is the presence of coronary artery disease (CAD) and left ventricular hypertrophy (LVH). It was hypothesized that N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and B-type natriuretic peptide (BNP) levels could identify CAD and LVH in asymptomatic patients with CKD. Clinical, laboratory, and echocardiographic data were collected prospectively in 54 ambulatory patients with CKD not requiring dialysis. CAD was defined by previous myocardial infarction or coronary revascularization. The median age was 70 years (interquartile range [IQR] 57 to 76). Fourteen patients (26%) had CAD, and 30 (56%) had LVH. Median NT-pro-BNP was 724 pg/ml (IQR 168 to 2,950), median BNP was 137 pg/ml (IQR 31 to 391), and the median glomerular filtration rate (GFR) was 31 ml/min/1.73 m2 (IQR 21 to 42). A strong correlation was found between NT-pro-BNP and BNP levels (R = 0.74, p <0.0001), but only moderate correlations were found between NT-pro-BNP and GFR (R = -0.45, p = 0.0006) and between BNP and GFR (R = -0.38, p = 0.005). There was no trend of an increase in the prevalence of LVH or CAD with decreasing GFR. However, across progressive NT-pro-BNP and BNP quartiles, the prevalences of LVH and CAD increased significantly. Receiver-operating characteristic curves showed that these 2 markers are similar and significant predictors for indicating LVH (area under the curve [AUC] 0.72, p = 0.005 for NT-pro-BNP; AUC 0.72, p = 0.007 for BNP) and CAD (AUC 0.80, p = 0.001 for NT-pro-BNP; AUC 0.82, p = 0.0004 for BNP; p = 0.45 for NT-pro-BNP vs BNP). In conclusion, NT-pro-BNP and BNP levels are significant and equivalent indicators of CAD and LVH in asymptomatic patients with CKD.

Hypertensive crisis: hypertensive emergencies and urgencies.

Hypertensive crisis is a serious condition that is associated with end-organ damage or may result in end-organ damage if left untreated. Causes of acute rises in blood pressure include medications,noncompliance, and poorly controlled chronic hypertension. Treatment of a hypertensive crisis should be tailored to each individual based on the extent of end-organ injury and comorbid conditions. Prompt and rapid reduction of blood pressure under continuous surveillance is essential in patients who have acute end-organ damage.

Coronary artery fistulas: clinical and therapeutic considerations.

Coronary artery fistulas vary widely in their morphological appearance and presentation. These fistulas are congenital or acquired coronary artery abnormalities in which blood is shunted into a cardiac chamber, great vessel, or other structure, bypassing the myocardial capillary network. The majority of these fistulas arise from the right coronary artery and the left anterior descending coronary artery; the circumflex coronary artery is rarely involved. Clinical manifestations vary considerably and the long-term outcome is not fully known. The patients with coronary fistulas may present with dyspnea, congestive heart failure, angina, endocarditis, arrhythmias, or myocardial infarction. A continuous murmur is often present and is highly suggestive of a coronary artery fistula. Differential diagnosis includes persistent ductus arteriosus, pulmonary arteriovenous fistula, ruptured sinus of Valsalva aneurysm, aortopulmonary window, prolapse of the right aortic cusp with a supracristal ventricular septal defect, internal mammary artery to pulmonary artery fistula, and systemic arteriovenous fistula. Although noninvasive imaging may facilitate the diagnosis and identification of the origin and insertion of coronary artery fistulas, cardiac catheterization and coronary angiography is necessary for the precise delineation of coronary anatomy, for assessment of hemodynamics, and to show the presence of concomitant atherosclerosis and other structural anomalies. Treatment is advocated for symptomatic patients and for those asymptomatic patients who are at risk for future complications. Possible therapeutic options include surgical correction and transcatheter embolization. Historical perspectives, demographics, clinical presentations, diagnostic evaluation, and management of coronary artery fistula are elaborated.

Firsts in cardiology: milestones and vital discoveries.

The modern day cardiology practice thrives on the extraordinary discoveries made in the understanding of the cardiovascular science and in the development of diagnostic and therapeutic methods. In this paper, the milestones and vital discoveries in the field of cardiology are described in chronologic order.

Cardiac effects of acute myelitis.

Neurogenic stunned myocardium has been described in association with subarachnoid hemorrhage, Guillain-Barre syndrome, and metastatic brain tumors. We describe a case of neurogenic stunned myocardium associated with acute myelitis. A 27-year-old female presented with acute onset of quadriplegia, sensory deficit, and acute pulmonary edema. Magnetic resonance imaging was consistent with acute myelitis. Echocardiogram showed left ventricular ejection fraction of 35% with moderate to severe global hypokinesis. During the course of admission, she had several episodes of sinus bradycardia and high degree atrioventricular block. All cardiac abnormalities resolved completely in eight days of admission.

Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism.

The role of electrocardiography in identifying right ventricular (RV) dysfunction in acute pulmonary embolism (APE) was evaluated in 81 patients with APE. The electrocardiographic markers studied were T-wave inversion in leads V1 to V3, the S1Q3T3 pattern, right bundle branch block, and sinus tachycardia. T-wave inversion in leads V1 to V3 had the greatest sensitivity and diagnostic accuracy for identifying RV dysfunction in patients with APE. The S1Q3T3 pattern and right bundle branch block had good specificity but moderate accuracy.

Role of postoperative vasopressor use in occurrence of atrial fibrillation after coronary artery bypass grafting.

Vasopressor use is common after coronary artery bypass grafting surgery. This study evaluated the role of postoperative vasopressor use as a predictor of occurrence of atrial fibrillation after coronary artery bypass grafting and demonstrates that vasopressor use is an independent predictor of such an occurrence.

Role of biochemical markers in diagnosis of myocardial infarction.

An ideal cardiac biochemical marker should have not only high sensitivity but also high specificity to myocardial infarction. The creatine kinase-MB, a relatively specific cardiac marker, could be elevated in situations other than acute myocardial infarction, such as renal failure, muscular injury, and myopathy. Although these are more specific than creatine kinase-MB, cardiac troponins have also been reported to be elevated in conditions other than acute myocardial infarction, such as chronic renal failure, acute myocarditis, cardiomyopathy, congestive heart failure, pulmonary embolism, rhabdomyolysis, sepsis, and left ventricular hypertrophy. With the ongoing research in this field, future holds hopes of finding an ideally specific marker of myocardial infarction, but until then biochemical markers should be used in conjunction with clinical assessment and electrocardiography in making the diagnosis of myocardial infarction, and the patients should not be treated merely on the basis of elevated serum levels of cardiac biochemical markers.

Prolonged QT interval with markedly abnormal ventricular repolarization in diphenhydramine overdose.

Diphenhydramine is a histamine-1 receptor antagonist of ethanolamine origin with anticholinergic, sedative, antivertigo, antiemetic, antidyskinetic, and local anesthetic properties. It inhibits the fast sodium channels and, at higher concentrations, also the potassium channels, inhibition of which may result in QT interval prolongation on electrocardiogram. The markedly abnormal ventricular repolarization is rare with diphenhydramine overdose. We report a case where a young woman who took moderate overdose of diphenhydramine (625 mg) along with acetaminophen developed prolonged QT interval with strikingly abnormal T waves. These changes reverted to normal with treatment. Patient did not experience torsade de pointes, possibly secondary to the protective effect of the diphenhydramine overdose-related tachycardia. As the tachycardia caused by diphenhydramine overdose seems to protect against torsade de pointes, it may be practical to avoid bradycardia in acute phase of diphenhydramine toxicity. Acetaminophen has not been shown to prolong QT interval or effect cardiac repolarization.

Clinical perspectives of the primary spontaneous coronary artery dissection.

Spontaneous coronary artery dissection is a rare cause of acute coronary syndrome or sudden death. Typically it affects young women during the peripartum period and those using oral contraceptives. The pathophysiology remains unclear, but an eosinophilic periadventitial inflammation has been commonly observed in such cases. Unlike atherosclerotic intimal dissection, the dissection plane in the spontaneous dissection lies within the media or between the media and adventitia. Due to the rarity of the condition, the optimal management of the spontaneous coronary artery dissection has not been established and it may range from conservative medical treatment to percutaneous or surgical interventions depending upon the anatomy of the dissection, compromise of the vessel lumen and the clinical circumstances. The reported prognosis varies widely. Spontaneous coronary artery dissection should be considered in the differential diagnosis in young persons with precordial chest pain, especially women in the peripartum state and those using oral contraceptives. The clinical perspectives of the primary spontaneous coronary artery dissection are elaborated.

Evolution of the theory of circulation.

The first known descriptions regarding the basic aspects of circulation was probably in 500 B.C., by the Greek thinker Alcmaeon of Croton who observed arteries and veins to be dissimilar in animal dissection, and this was followed by the description of the human heart as a three chambered organ by Aristotle in 350 B.C. Herophilus of Chalcedon, a Greek anatomist, confirmed the findings of dissimilarity between arteries and veins in human cadaver dissections in 300 B.C., and determines that arteries were thicker than veins and contained blood. The advancement by far in the learning of human circulation was made possible first by significant contribution of Galen followed by observations of Ibn al-Nafis, Servetus, Colombo, Cesalpino, Vesalius and Fabricius. In 17th century William Harvey, an English physician, made important advancements into the understanding of this important area of medicine, advancements that continued with the observations of Malpighi.

Long QT syndrome and torsade de pointes in transient left ventricular apical ballooning syndrome.

A recently reported cardiac syndrome of reversible left ventricular apical ballooning, also called Takotsubo cardiomyopathy or ampulla cardiomyopathy, clinically resembles acute myocardial infarction and presents with chest pain, anterior electrocardiographic changes and minimal elevation of cardiac enzymes in absence of myocardial ischemia or injury. Left ventricular function recovers completely in days to weeks. This syndrome is likely a non-ischemic, metabolic-dependent syndrome caused by stress-induced activation of the cardiac adrenoceptors, and results in markedly abnormal ventricular repolarization. Reported here is a case of left ventricular apical ballooning syndrome with QT interval prolongation in a young man who developed torsade de pointes and experienced aborted sudden cardiac death. Patient had a complete recovery of cardiac function and normalization of QT interval in a few days. The syndrome of transient left ventricular apical ballooning could be considered among the causes of long QT syndrome and torsade de pointes.

Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis.

Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.

Left main coronary artery aneurysm.

Left main coronary artery aneurysm is rare finding at coronary angiography. We report a case of a large left main coronary artery aneurysm in a 59-year-old male who had cardiac catheterization for effort angina and inducible myocardial ischemia.

Staphylococcus aureus infective endocarditis and septic pulmonary embolism after septic abortion.

We report a case of a 26-year-old female who after septic abortion developed tricuspid valve endocarditis with large vegetations, which subsequently resulted in embolism to right main pulmonary artery. Patient was treated with intravenous antibiotics and had a good recovery.

Transient left ventricular apical ballooning: a novel heart syndrome.

A novel cardiac syndrome of left ventricular apical ballooning (Takotsubo cardiomyopathy-ampulla cardiomyopathy) involves reversible left ventricular apical ballooning (during systole) of acute onset with chest pain, electrocardiographic changes, and minimal elevation of cardiac enzymes resembling acute myocardial infarction, but without evidence of myocardial ischemia or injury. Patients have no angiographic evidence of coronary artery stenosis and there is almost always a complete recovery of left ventricular function in days to weeks. The precise etiologic basic of this syndrome is not clear but most likely it is a non-ischemic, metabolic syndrome caused by stress-induced activation of the cardiac adrenoceptors in absence of ischemia and reperfusion. Reported here is a case of stress-induced transient left ventricular apical ballooning syndrome in a young woman.

Treatment of refractory angina pectoris.

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.

Cardiac troponin I release in acute pulmonary embolism in relation to the duration of symptoms.

PURPOSE: To evaluate the release of cardiac troponin I in normotensive patients with acute pulmonary embolism in relation to the duration of symptoms. METHODS: Fifty-seven normotensive patients with acute pulmonary embolism were included in the study. Patients were divided into two groups based on the duration of symptoms at presentation: symptoms of < or =72 h, group A; symptoms of >72 h, group B. Serum cardiac troponin I levels were measured at presentation. RESULTS: Mean age was 63+/-18 years and 23 (40%) patients were males. Thirty-three (58%) patients had symptoms of < or =72 h (group A) and 24 (42%) had symptoms of >72 h (group B). Both groups had similar prevalence of right ventricular dysfunction on echocardiography (55% [n=18] in group A vs. 42% [n=10] in group B, p=NS). Sixteen patients had elevated serum cardiac troponin I (mean+/-S.D. 3.3+/-2.3 ng/ml, range 0.6-8.3 ng/ml). Elevated serum cardiac troponin I was strongly associated with right ventricular dysfunction (p=0.015). All patients with elevated serum cardiac troponin I (n=16) were in group A (p<0.0001). Twelve of 18 (67%) patients with (p=0.0005) and 4 of 15 (27%) patients without (p=NS) right ventricular dysfunction had elevated serum cardiac troponin I. Thirteen of 16 (81%) patients with elevated serum cardiac troponin I had duration of symptoms < or =24 h at presentation. CONCLUSIONS: The dynamics of cardiac troponin I release in acute pulmonary embolism in patients who present with symptoms of < or =72 h duration could be different from those who present with longer duration of symptoms. Therefore, the use of cardiac troponin I in risk stratification of acute pulmonary embolism might be limited to the patients presenting within 72 h of the onset of symptoms.

Acute pulmonary embolism in elderly: clinical characteristics and outcome.

OBJECTIVE: To evaluate the clinical characteristics and outcome of acute pulmonary embolism in elderly in comparison to the younger patients. METHODS: Study population consisted of 136 patients with a confirmed diagnosis of acute pulmonary embolism. Clinical characteristics and thromboembolic risk factors were analyzed between the elderly (> or =65 years of age) and the younger (<65 years of age) patients. In-hospital mortality was used as a measure of outcome. RESULTS: Elderly group consisted of 70 patients (age 76.4+/-8.3 years, range 65-96 years; females 58%) and younger group of 66 patients (age 48.5+/-12 years, range 18-64 years, females 59%). Syncope was more frequent in elderly group (19% vs. 6%, P=0.03) but the symptoms of shortness of breath and pleuritic chest pain were not significantly different between groups. Malignancy was the most common risk factor for thrombo-embolism, but immobilization predominated among patients in elderly group (21% vs. 6%, P=0.01). Tachycardia was common in younger patients compared to the elderly. Ventilation-perfusion scan was used more commonly in younger patients (76% vs. 57%, P=0.02), whereas, helical computed-tomography scan was used equally in both groups. Most of the patients had lower extremity duplex study (97% in each group). Inferior vena cava filter placement was common and thrombolytic therapy rare among elderly patients. Patients in elderly group had higher in-hospital mortality (17% vs. 5%, P=0.02). CONCLUSIONS: Syncope is a more frequent presenting symptom and immobilization a common risk factor in elderly patients with acute pulmonary embolism. In addition, they have higher in-hospital mortality.

Internal mammary artery steal syndrome secondary to an anomalous lateral branch.

A 53-year-old male who underwent three-vessel coronary artery bypass grafting had a left internal mammary artery (LIMA) graft to the left anterior descending artery (LAD) and saphenous venous grafts to right coronary artery (RCA) and left circumflex coronary artery. Four years after surgery, he developed exertion angina associated with upper body exercises and even deep breathing at times. Angiographic evaluation revealed an anomalous lateral internal thoracic artery with steal phenomenon documented by adenosine cardiolyte. Patient was successfully treated with transcutaneous steel coil embolization by closing the anomalous vessel. Repeat stress electrocardiogram did not show any signs of ischemia. This case report emphasizes the variability in internal mammary artery (IMA) anatomy and the need to completely ligate all the branches of internal mammary artery intraoperatively.