PubMed Health⌕ Search

Biomedical subjects

Amal Mattu

Publications and source records attributed to Amal Mattu.

8 recordsLinked to original sources

The Brugada syndrome.

Brugada syndrome describes the syndrome of sudden cardiac death in the setting of the following electrocardiographic findings: right bundle branch block pattern with ST-segment elevation in the right precordial leads. The right bundle branch block may be incomplete while the ST segment elevation is minimal. The electrocardiographic findings are not constant. Patients suspected of having Brugada syndrome should be promptly referred for electrophysiological testing and treatment. Rapid referral and placement of an implantable cardioverter defibrillator (ICD) is associated with an excellent prognosis, whereas failure to diagnose this condition is associated with a high risk for sudden death. Therefore, it is imperative that all emergency physicians be familiar with the typical ECG manifestations of Brugada syndrome. Three illustrative cases are presented with a review of the syndrome.

Adult↗

Malaria: a rising incidence in the United States.

Malaria is frequently a deadly disease, particularly in tropical countries of the world where this protozoan infection is endemic. While physicians in tropical countries are familiar with the presentation, those who do not practice in endemic regions of the world may neglect to add tropical diseases to their differential diagnosis of fever. Epidemiologic data from the CDC show the number of cases of malaria being diagnosed in the United States in the last decade has risen sharply. With international travel continuing to rise, there is strong reason to consider malaria as a source of fever.

Antimalarials↗

Serum phosphate abnormalities in the emergency department.

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.

Blood Chemical Analysis↗

Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient.

Inverted T waves produced by myocardial ischemia are classically narrow and symmetric. T-wave inversion (TWI) associated with an acute coronary syndrome (ACS) is morphologically characterized by an isoelectric ST segment that is usually bowed upward (ie, concave) and followed by a sharp symmetric downstroke. The terms coronary T wave and coved T wave have been used to describe these ischemic TWIs. Prominent, deeply inverted, and widely splayed T waves are more characteristic of non-ACS conditions such as juvenile T-wave patterns, left ventricular hypertrophy, acute myocarditis, Wolff-Parkinson-White syndrome, acute pulmonary embolism, cerebrovascular accident, bundle branch block, and later stages of pericarditis.

Adult↗

The prominent T wave: electrocardiographic differential diagnosis.

The prominent T wave is an abnormal T-wave morphology encountered in the earliest phase of ST-segment elevation acute myocardial infarction (AMI). Prominent T waves, however, are associated with other diagnoses, including hyperkalemia, early repolarization, and left ventricular hypertrophy (LVH). This article focuses on the electrocardiographic differential diagnosis of the prominent T wave with the presentation of 4 illustrative cases. We also recommend that the designation hyperacute should refer exclusively to the prominent T waves of ST-segment elevation AMI.

Adult↗

Electrocardiographic manifestations of hypothermia.

Hypothermia is generally defined as a core body temperature less than 35 degrees C (95 degrees F). Hypothermia is one of the most common environmental emergencies encountered by emergency physicians. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. The classic and well-known electrocardiographic (ECG) manifestations of hypothermia include the presence of J (Osborn) waves, interval (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known (ECG) findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. Hypothermia can also blunt the expected ECG findings associated with hyperkalemia. A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia.

Adult↗

Electrocardiographic ST segment elevation: left ventricular aneurysm.

Left ventricular aneurysm (LVA), also described as dyskinetic left ventricular segment, is defined as a localized area of infarcted myocardium that bulges outward during both systole and diastole. LVAs most often are noted after large anterior wall events but may also be encountered status after inferior and posterior wall injuries. In most cases, LVA is manifested electrocardiographically by varying degrees of ST segment elevation (STE), which may be difficult to distinguish from ST segment changes caused by acute myocardial infarction. The STE is generally associated with well-developed, completed Q waves in the anterior precordial leads, and there will not be reciprocal ST depression in the contralateral leads. This article focuses on the electrocardiographic findings useful in making the diagnosis of left ventricular aneurysm as well as distinguishing LVA from other STE syndromes.

Aged↗

Electrocardiographic manifestations of Wellens' syndrome.

Wellens' syndrome is a pattern of electrocardiographic T-wave changes associated with critical, proximal left anterior descending (LAD) artery stenosis. The syndrome is also referred to as LAD coronary T-wave syndrome. Syndrome criteria include T-wave changes plus a history of anginal chest pain without serum marker abnormalities; patients lack Q waves and significant ST-segment elevation; such patients show normal precordial R-wave progression. The natural history of Wellens' syndrome is anterior wall acute myocardial infarction. The T-wave abnormalities are persistent and may remain in place for hours to weeks; the clinician likely will encounter these changes in the sensation-free patient. With definitive management of the stenosis, the changes resolve with normalization of the electrocardiogram. It is vital that the physician recognize these changes and the association with critical LAD obstruction and significant risk for anterior wall myocardial infarction.

Coronary Stenosis↗