A Rare Case of Takotsubo Cardiomyopathy in a Patient With No Identifiable Emotional or Physical Stressors.

Takotsubo cardiomyopathy (TCM) is a cardiac condition that presents with features of acute myocardial infarction and transient systolic dysfunction without angiographic findings of obstructive coronary heart disease. Common presenting symptoms include acute substernal chest pain, dyspnea and syncope. It is usually triggered by recent emotional or physical stress such as head trauma, stroke, sepsis, overproduction of catecholamines such as pheochromocytoma or following Myasthenia crisis. We are here to report a case of TCM who does not have any identifiable emotional or physical stress prior to the event. The patient was a 76-year-old Caucasian female with a past medical history of hypertension who presented to the hospital with chest pain which initially was treated as non-ST elevation myocardial infarction (NSTEMI) with aspirin, ticagrelor and heparin infusion. Cardiac catheterization later revealed non-obstructive coronary artery disease but showed akinesis of inferior, apical and anterior walls with hyperdynamic basal segments indicating TCM.

A Case of Three-Vessel Coronary Artery Disease Associated With Marijuana Use.

Marijuana is one of the most popular psychotropic drugs among adolescents and young adults. With the recent surge in marijuana use across the United States, it is very important for physicians to understand the clinical implications associated with marijuana use. In this case report, we discuss a case of a young adult who presented to the emergency department with chest pain and was found to have three-vessel coronary artery disease (CAD). The patient did not have any significant past medical history or family history of cardiac diseases but reported a significant history of marijuana use. This case report aims to add to the growing area of research on the association between myocardial infarction (MI) and marijuana use.

Coronary Artery Ectasia: A Case Report Discussing the Causes, Diagnosis, and Treatment.

The localized or diffused dilation of a coronary artery lumen is referred to as coronary artery ectasia (CAE). Though it is well recognized, CAE is a rare finding that is encountered in the diagnostic procedure of coronary angiography. This form of atherosclerotic coronary artery disease (CAD) can be found in 1.4-4.9% of all coronary angiography patients. CAE can manifest in combination with stenotic lesions or present as an isolated condition. Its risk factors are similar to those of atherosclerosis. The underlying pathophysiology involves a vascular remodeling response to atherosclerosis. Enzymatic degradation by matrix metalloproteinases (MMP) and accumulation of lipoproteins play an important role in the remodeling process. CAE can be diagnosed with the help of imaging modalities such as coronary CT angiogram (CTA) and coronary magnetic resonance angiogram (MRA); coronary angiography is considered the gold standard procedure. The management strategies include treating the cardiovascular risk factors, prevention of thromboembolic events, and percutaneous/vascular revascularization. CAE can be managed medically, but percutaneous/surgical revascularization [coronary artery bypass grafting (CABG)] is an option to treat patients with co-existing symptomatic obstructive lesion refractory to medical treatment. Further trials are required to optimize the management guidelines related to CAE. In this report, we describe the case of a 42-year-old man with a past medical history of hypertension, hyperlipidemia, and asthma who presented with shortness of breath and minimally elevated troponin level. Coronary angiography revealed three vessels with ectasia and severe left ventricular dysfunction on ventriculography.

The Myth of Colchicine in Treating Myopericarditis: Case Report and Literature Review.

Myopericarditis is inflammation of the pericardium with concurrent myocardial involvement. The clinical presentation of myopericarditis is often with varying degrees of cardiac symptomatology. Its etiology is often idiopathic, but it may also be related to infectious and inflammatory prodrome. Symptoms are proportional to the extent and pattern of myocardial involvement. Many are diagnosed sub-clinically during the management of other systemic illnesses. Echocardiography and cardiac magnetic resonance imaging are important tools in the evaluation of myopericarditis, as the diagnosis of left ventricular dysfunction greatly affects the management, follow-up, and prognosis of these patients. The acute management of myopericarditis remains without clear direction and focuses on symptom control. The use of NSAIDs is often cautioned, as it has been described to actually accelerate the myocarditic process in animal models, possibly increasing mortality. Colchicine, a well-established anti-inflammatory agent, may have a role in the management of acute myopericarditis. We present two cases, each involving a young male, without underlying medical conditions, who presented to the emergency room with acute onset chest pain. Both were found to have elevated cardiac biomarkers and electrocardiographic (EKG) changes, admitted as in-patients and eventually diagnosed with acute myopericarditis. They made full recoveries and were eventually discharged home. Both were started on colchicine during hospitalization, which were continued for several months upon discharge. Overall, there is limited published data regarding the medical management of myopericarditis. There need to be prospective studies and registries to further our knowledge in the management of this illness.

Unusual Troponin Level in Atrioventricular Nodal Reentrant Tachycardia Despite Normal Coronary Arteries.

BACKGROUND Elevation of troponin in atrioventricular nodal reentrant tachycardia may occur but it is usually mild. Although there are often no identifiable etiologies, stimulants and excessive activities have been implicated. CASE REPORT We present the case of a 36-year-old female with palpitations. Her laboratory investigation was positive for a very high level of troponin despite insignificant illicit drug use, unremarkable inflammatory markers, unremarkable coronary arteries after a coronary angiogram, and normal biventricular function without gadolinium enhancement on cardiac magnetic resonance imaging. The only attributable culprit was atrioventricular nodal reentrant tachycardia during electrophysiology studies but radiofrequency ablation was unsuccessful. We believe it is important that physicians should be aware that a very high troponin does not always reflect an infarction or structural damage to the heart. CONCLUSIONS It has been documented that tachyarrhythmias cause a mild increase of troponin levels and severe elevations of troponin are often attributed to myocardial infarction. Physicians should be aware that troponin may increase to over 200 times above the normal limit in a patient with atrioventricular nodal reentrant tachycardia, normal coronary arteries, and no structural heart disease.

An Obstructed Anomalous Left Anterior Descending Coronary Artery Arising from the Right Coronary Artery Requiring Surgical Intervention.

A 47-year-old female presented to our hospital with symptoms of stable angina. Cardiac catheterization revealed a rare coronary artery anomaly of the left anterior descending (LAD) artery branching off the right coronary artery ostium. Furthermore, the anomalous LAD artery exhibited significant atherosclerotic obstruction. Our review of the literature found only nine such previously described cases. Due to the unique nature of coronary artery anomalies and their complications, we would like to contribute our case to the medical literature.

The effect of lower body weight support on arterial wave reflection in healthy adults.

Body weight support (WS) during treadmill exercise is used to rehabilitate orthopedic/neurological patients. WS lowers musculoskeletal strain and load. It compresses the lower body and increases intrathoracic volume. We studied short-term effects of WS on wave reflection indices using applanation tonometry during progressive WS of 25%, 50%, and 75% of body weight in 25 healthy men. WS decreased mean heart rate from 79 to 69 beats/min (P < .001). Peripheral and central mean arterial, systolic, and pulse pressures (PP) remained unchanged. There was a trend toward lower peripheral and central diastolic pressure. PP amplification ratio decreased significantly (P = .005). Reflected wave characteristics: Augmented pressure and index increased in a stepwise manner with WS (both P < .001). Both ejection duration and systolic duration of the reflected pressure wave (Ätr) increased progressively (both P < .001). The round-trip travel time (Δtp) was unchanged. Left ventricular workload and oxygen demand: Left ventricular wasted pressure energy increased (P < .001), and the subendocardial viability ratio decreased (P = .005), whereas the tension time index remained unchanged. In normal men, WS acutely decreases the PP amplification ratio, increases the amplitude and duration of the reflected aortic pressure wave, and increases measures of wasted left ventricular pressure energy and oxygen demand.

Comparison of passive leg raising and hyperemia on macrovascular and microvascular responses.

Passive leg raising is a simple diagnostic maneuver that has been proposed as a measure of arterial vasodilator reserve and possibly endothelial function. While passive leg raising has previously been shown to lower blood pressure, increase flow velocity and cause brachial artery dilation, its effects on microvascular flow has not been well studied. Also, passive leg raising has been directly compared previously to upper arm but never to lower arm occlusion of blood flow induced hyperemia responses. We compared changes in macrovascular indices measured by brachial artery ultrasound and microvascular perfusion measured by Laser Doppler Flowmetry induced by passive leg raising to those provoked by upper arm and lower arm induced hyperemia in healthy subjects. Upper arm induced hyperemia increased mean flow velocity by 398%, induced brachial artery dilatation by 16.3%, and increased microvascular perfusion by 246% (p<.05 for all). Lower arm induced hyperemia increased flow velocity by 227%, induced brachial artery dilatation by 10.8%, and increased microvascular perfusion by 281%. Passive leg raising increased flow velocity by 29% and brachial artery dilatation by 5.6% (p<.05 for all), but did not change microvascular perfusion (-5%, p=ns). In conclusion, passive leg raising increases flow velocity orders of magnitude less than does upper arm or lower arm induced hyperemia. Passive leg raising-induced brachial artery dilatation is less robust than either of these hyperemic techniques. Finally, although upper arm and lower arm hyperemia elicits macrovascular and microvascular responses, passive leg raising elicits only macrovascular responses.