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Biomedical subjects

Ijaz A Khan

Publications and source records attributed to Ijaz A Khan.

At least 19 recordsLinked to original sources

Clinical aspects of the Chagas' heart disease.

Chagas' heart disease, caused by protozoan Trypanosoma cruzi, is a common cause of cardiomyopathy in the Americas. Transmission of T. cruzi occurs through Reduviids, the kissing bugs. Less common ways of transmission are blood transfusion, congenital transmission, organ transplantation, laboratory accident, breastfeeding, and oral contamination. Infestation results in cardiac dysautonomia, myocardial apoptosis, and myocardial fibrosis. In acute phase, death is mostly caused by myocarditis and in chronic phase, it is mostly by irreversible cardiomyopathy. A majority of the patients with Chagas' disease remain in the latent phase of disease for 10 to 30 years or even for life. Specific anti-Chagas' therapy with trypanocide drugs is useful in acute phase but the management of chronic Chagas' heart disease is mostly empirical. The mortality during the acute phase of cardiac Chagas is around 5%. Five-year mortality of chronic Chagas' disease with cardiac dysfunction is above 50%. The clinical aspects of the Chagas' heart disease are concisely reviewed.

Acute Disease↗

Cardiac troponin I release in non-ischemic reversible myocardial injury from parvovirus B19 myocarditis.

Cardiac troponin I is released from myocytes in both reversible and irreversible myocardial injury. The changes in myocyte membrane permeability resulting from the injury could be enough for the release of cardiac troponins from the free cytosolic pool of myocytes without structural damage. We report a case of parvovirus B19 myocarditis in a 26-year-old male who developed regional wall motion abnormalities and severe left ventricular systolic dysfunction with elevated serum levels of cardiac troponin I (peak=11.7 ng/ml). Diagnosis of parvovirus myocarditis was confirmed by presence of high titers of parvovirus B19 IgG and identification of parvovirus B19 DNA by polymerase chain reaction. Within a few days of supportive treatment, the regional wall motion abnormalities resolved, the cardiac function recovered, and the elevation in serum cardiac troponin I subsided. This case further denotes the possibility of release of cardiac troponin I in non-ischemic, reversible myocardial injury.

Adult↗

Electrocardiographic changes in combined electrolyte depletion.

Cardiac action potential is affected by extracellular gradients in potassium, calcium, and magnesium with resultant electrocardiographic changes varying from subtle findings to marked repolarization abnormalities. This report presents marked electrocardiographic changes resulting from a combination of electrolytes depletion in a patient with bulimia and anorexia nervosa.

Adult↗

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.

Aged↗

Thoracoabdominal aortic aneurysm: diagnosis and management.

Thoracoabdominal aortic aneurysm is defined as a focal and localized dilatation of the aorta 1.5 to 2 times the diameter of the normal adjacent aorta and containing all three layers of the arterial wall. Conventional open surgical repair remains the gold standard for the majority of the patients with thoracoabdominal aortic aneurysm. Endovascular stent-graft aortic repair is a promising emerging therapy, which at present is considered an alternative to surgery in the elderly and in those with significant comorbid conditions. Adjunctive beta-blocker therapy should be used in all patients to reduce the shear force on the aortic wall.

Journal Article↗

Hypothermia: evaluation, electrocardiographic manifestations, and management.

Hypothermia-related cases typically occur after exposure to low ambient temperatures; however, numerous cases occur in individuals with no history of exposure to cold environment. Hypothermia is associated with such complications as acidosis, impaired myocardial function, bleeding diathesis, and decreased kidney and liver function. The well-known electrocardiographic manifestations of hypothermia are the presence of J (Osborn) waves, prolonged PR, QRS, and QT intervals, and atrial arrhythmias. The choice of rewarming therapy is based on the degree of hypothermia. The evaluation, electrocardiographic manifestations, and management of hypothermia are reviewed.

Acidosis↗

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.

Angiotensin-Converting Enzyme Inhibitors↗

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.

Aortic Dissection↗

Hyperkalemia induced failure of atrial and ventricular pacemaker capture.

Hyperkalemia is a life threatening metabolic condition. The common risk factors for hyperkalemia include renal insufficiency, use of angiotensin converting enzyme inhibitors, potassium supplementation and excessive consumption of potassium containing diet. A mild to moderate increase in serum potassium causes an increase in myocardial excitability, but further increase leads to impaired myocardial responsiveness, including that to pacing stimulation. Hyperkalemia has been reported to cause failure of atrial capture due to pacemaker exit block. We report a case where hyperkalemia resulted in failure of both the atrial and the ventricular pacemaker capture.

Electrocardiography↗

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.

Cardiac Catheterization↗

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.

Biomarkers↗

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.

Arterio-Arterial Fistula↗

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.

Cardiology↗

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.

Acute Disease↗

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.

Acute Disease↗

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.

Adult↗