Tagged with "identity Archives - The Braindoc's Blog"

“That Achy Breaky Heart”:Rewriting Tags


Your Achy Breaky Heart


Thus, Lady! will it be with me,

And I must view thy charms no more;

For, while I linger near to thee,

I sigh for all I knew before.

In flight I shall be surely wise,

Escaping from temptation’s snare:

I cannot view my Paradise

Without the wish of dwelling there.
-Lord Byron


Michelangelo, Fall and Expulsion from Garden of Eden

“Tis better to have loved and lost,
Than never to have loved before”

So the saying goes. Even though you know it makes a lot of head sense, it is the heart that takes the brunt of the punishment. I remember days of seeking solitude, trying to find a dark corner somewhere to lick my open wounds from a recent romantic loss. I remember how the world, the environment, my common routes of travel lost its vibrant color, lost its joyous song, broke its warm embrace with my lively hopes. Everything that shines with colorful brilliance while was shared, seemed shadowed by dismal gray, aloof, cold and dead after love’s loss.

It was at such a time when an ember of unquenched curiosity remained hot in the ashes of my despair. It was the remnant of my ongoing fascination and wonder of who we are as people, our design, our fixed sense of being and the organic design of our identity that remained. I have always found the and its seat in the as a most profound and beautiful construct. As I reflected on the commonplace of despair within the social struggles of our world, I knew that something yet remains that keeps us moving forward, hoping, believing in the possibility of better days. In that journey, time would surely numb the time pinned moments of injury or insult. Emotional pain, though heavy and enduring does not forever obstruct life’s view. It will not forever weigh your heart down, drain your energy and dominate the table of your mental occupations. Such intensity of emotion clearly affects our physical being. I have posted a graphic about this below.


The beauty and the curse of memory is that it is a lingering of an otherwise time-fixed event. The very mechanics which make two hearts fonder over time is the same which brings up fears and hurts. Every event and a memorable moment is never a completely fresh experience. We bring something of our experiences into the moment and mix it with the present dynamic. Every event, though shared with another, no matter how similar, will have an interpretation different. When we spend time with a partner, we share in the experience. Therefore, even places, people, colors, nearly anything that strikes our senses can be shaded by those we have shared the experience. In other words, the emotional memory tag is connected to each item. That is why we may suffer a loss of someone dear but feel bombarded by memories of the cherished loss frequently. We often do not realize how a tag can activate other tags from other experiences.

The tags of shared comfort, pleasure and joy will hang from many objects of your present scenes. Close behind the vague mass of memories’ reflexive joy called forward is the cold stinging pain of loss that tears through your soul, stopping your breath in a renewed shock as you moan with breaths release. As the cycling pain of labor, prepares for new life at birth, so is the release of burdens and loss vital, if life is to be reclaimed.

So in my darker hours, I found myself comforted by my intrigue. I shifted in the seat of a victim and companioned my sorrow as a student. I fanned my glowing embers of fascination into a fire that grew greater than the fire of loss that threatened to consume me. Soon there was something within that released its grip of fear as I rose to stand above the pain. The experience became the subject and I became the experience again. I sighed in release and felt a momentary shift of ‘normalcy’ once again. I knew then that is was possible to move past this experience. That was enough for that moment. I was grateful.



I knew it would take time. I knew the waves would return. There will be ups and downs, ebbs and flows. But I would eventually get past it. Tags need to rewritten, places redefined and people rediscovered. Yes, it is a painstaking, long and difficult process. But change will come, not all at once, but in small steps. It takes time. Friends and activities clearly help. Even when you do not feel sociable or you do not have any pleasure of activities that once brought joy, it is important to just turn from the dark corner of lonely isolation. Sometimes grabbing a book and sitting at a more public arena is enough to crack open the redefining life before you, in order for you to continue. For the goal is not to forget what was lost. That is not why we have such circuitry. We have this design to aid us in making life more real, more colorful, more lively. Only when we understand what it is to have sorrow, will we be equipped for joy. Losing someone dear permits our overstimulated minds to prioritize what really matters. Not for our harm, but for our good. Valuing the good in others help to sensitize our focus for quality in each other.


Once you grasp the concept of memory tags and how it plays a significant part in painful memory of loss, you will appreciate the process of getting through the tough times. As pointed out, it is the memory tags attached to people, places and things that stir up memories of loss. We will not always understand why hurts are necessary, but without pain, we would never enjoy pleasure. For me, remembering my loved ones are important for my growth, my habits of life. I know the good that was shared is forever a part of me as well. This makes my eyes more fixed on the good and more important matters of life and living.
For those that seclude themselves and hide away from the world, the tags which were shared will remain relatively fixed. Life can be arrested in place. There will be no recovery and no expectation for improved quality of life. But to continue to experience people, places and things with others who had not shared your unique experience, you will be able to broaden the memory tags which they bear. Life will get easier, and much can be gained by enriching others by your fond memories. As once quoted, “A great friend can half your sorrow and double your joy”.

For those who suffer loss. I pray for your comfort. But Remember RIP; (Remember In Perspective).

Thanks for sharing my walk.


How Does Affect Us?


The very real, heart of Sorrow…


Takotsubo Cardiomyopathy, or Broken-Heart Syndrome

This article has been cited by other articles in PMC.

Takotsubo cardiomyopathy mimics acute coronary syndrome and is accompanied by reversible left ventricular apical ballooning in the absence of angiographically significant coronary artery stenosis. In Japanese, “tako-tsubo” means “fishing pot for trapping octopus, ” and the left ventricle of a patient diagnosed with this condition resembles that shape. Takotsubo cardiomyopathy, which is transient and typically precipitated by acute emotional , is also known as “stress cardiomyopathy” or “broken-heart syndrome.”

Herein, we describe the clinical angiographic characteristics of 4 patients who exhibited this syndrome, and we review the existing literature and propose reasons to conduct prospective studies.

Key words: Cardiomyopathies/diagnosis/etiology/physiopathology, catecholamines/secretion, chest pain/etiology, coronary angiography, coronary disease/physiopathology, echocardiography, electrocardiography, heart/physiopathology, myocardial ischemia/diagnosis, stress, psychological/complications/physiopathology, takotsubo cardiomyopathy, ventricular dysfunction, left/diagnosis/etiology/physiopathology
Takotsubo cardiomyopathy mimics acute coronary syndrome. It is accompanied by reversible left ventricular (LV) apical ballooning in the absence of angiographically significant coronary artery stenosis. In Japanese, “tako-tsubo” means “fishing pot for trapping octopus, ” because the LV of a patient diagnosed with this condition resembles that shape. A transient entity typically precipitated by acute emotional stress, takotsubo cardiomyopathy is also called “stress cardiomyopathy” or “broken-heart syndrome.” Several cases of this interesting cardiomyopathy have been reported in Japan,1–8 and more recently in the United States9–13 and Belgium.14 Herein, we describe the clinical and angiographic characteristics of 4 patients diagnosed with takotsubo cardiomyopathy, and we review the existing literature.

Case Reports

Patient 1

A 57-year-old black woman with a history of hypertension and dyslipidemia was hospitalized because of the sudden onset of angina-like chest pain and dyspnea.Auscultation revealed bilateral basilar crackles and an S3 gallop.Electrocardiography (ECG) showed ST-segment elevation of 1 mm in leads V1 through V3. The QT interval was prolonged.Levels of creatine kinase-MB and troponin T were mildly elevated. Echocardiography showed substantial apical dysfunction, preserved basal function, and no intraventricular pressure gradient. The patient underwent emergency cardiac catheterization, which disclosed nosubstantial epicardial coronary artery stenosis. Left ventriculography showed systolic ballooning of the apex and hypercontraction of the basal segment (Fig. 1). The patient was treated with aspirin, an angiotensin-converting enzyme inhibitor, a diuretic, and statins. Two weeks later, the ECG showed complete resolution of the ST-segment elevation and no Q-wave formation. Echocardiography revealed remarkable improvement of the apical wall motion abnormality and normalization of the ejection fraction. It was concluded that acute emotional stress after the death of a relative had precipitated the initial symptoms.

Fig. 1 Patient 1. Left ventricular angiography in systole ( A) and diastole ( B) shows apical ballooning and hypercontraction of the basal segments.
Patient 2

A 64-year-old black woman with a history of diabetes mellitus presented with severe angina-like chest pain.Deep negative T waves were seen on ECG. Her cardiac enzyme levels were mildly elevated. The patient was admitted with a diagnosis of acute non-ST-segment-elevation myocardial infarction. An echocardiogram showed apical dyskinesis, an ejection fraction of 0.45, and no intraventricular pressure gradient. The patient’s ongoing chest pain prompted emergency coronary angiography with intra-aortic balloon pump support. The angiogram revealed apical ballooning in systole with concomitantly increased contractility in the basal segments. The overall LV systolic function (LVSF) was mildly depressed. With medical therapy, the patient’s symptoms improved. Echocardiography after 1 week showed normalization of the systolic apical ballooning and the LVSF. When questioned, the patient revealed that she had recently experienced severe emotional stress due to financial instability.

Patient 3

A 44-year-old white man without a pertinent medical history underwent urgent coronary angiography because of acute chest pain and marked precordial T-waveinversions suggestive of acute myocardial ischemia.Coronary angiography showed no significant stenosis of the coronary arteries. A challenge with acetylcholine elicited no spasm of either the right or the left coronary artery.Left ventriculography showed systolic apical ballooning with mild basal hypercontraction. Levels of creatine kinase-MB and troponin T were mildly elevated. One week later, echocardiography showed complete resolution of the wall motion abnormality. Severe occupation-related emotional stress had preceded the onset of this patient’s symptoms.

Patient 4

A 64-year-old black woman with a history of hypertension and hyperlipidemia presented after 1 day of severe nausea and vomiting.An ECG showed ST-segment elevation and deep T-wave inversion in the anterior leads.The QTinterval was also prolonged (Fig. 2). The cardiac enzyme levels were mildlyelevated. Emergency cardiac catheterization disclosed no obstructive coronaryartery disease. Left ventricular angiography revealed apical ballooning in systolewith mild basal hypercontraction. The patient’s LVSF was moderately reduced. Two weeks later, results of echocardiography showed resolution of the apical wall motion abnormality and the LV systolic dysfunction. The patient had not experienced emotional distress before the onset of symptoms.

Fig. 2 Patient 4. A 12-lead electrocardiogram of a patient diagnosed with takotsubo cardiomyopathy shows ST-segment elevation and deep T-wave inversions in the anterior leads, in association with a prolonged QT interval.

These 4 cases exhibited most of the characteristics of takotsubo cardiomyopathy that have been described in the literature:

A preponderant occurrence of the syndrome in elderly or postmenopausal females 2,8–10
Onset consequent to acute emotional stress or an acute medical condition 2,7,8,11
ST-segment elevation or , or T-wave changes 1–11
A prolonged QT interval 2,11
A mild increase in cardiac enzymes 2,9,10
Typical akinesis of the apical and distal anterior wall together with hypercontraction of the basal wall 2,8–10
The occasional presence of transient intracavitary pressure gradients in some patients 2,8,10
A need for acute hemodynamic support in some cases 2,8,10
C omplete resolution of the apical wall motion abnormality and the depressed LVSF. 2,3,8,9,11
Although the exact pathogenesis of takotsubo cardiomyopathy remains unclear, various mechanisms have been proposed. Dote and associates1 suggested coronary vasospasm as the pathogenic mechanism; however, induction of coronary vasospasm by acetylcholine or ergonovine has yielded mixed results. In some series, vasospasm in at least 1 epicardial coronary artery was present in most patients,3,8 whereas Akashi and colleagues2 found no coronary vasospasm in patients who underwent an acetylcholine challenge. Multivessel coronary spasm would be required to account for the apical wall motion abnormality seen in this syndrome. Similarly, the duration of wall motion abnormality in takotsubo cardiomyopathy typically is longer than would be expected in conventional cases of coronary vasospasm.

The possibility of myocardial injury due to microvascular spasm has also been suggested.3 Ako and coworkers,15 by the use of an intracoronary Doppler wire technique, demonstrated microcirculation impairments in instances of transient LV hypocontraction. Although this is an interesting explanation, several factors challenge its causative potential. First, microscopic findings in some patients who had LV apical ballooning were different from those in patients who had myocardial ischemia. The most common pathologic finding in takotsubo cardiomyopathy, focal catalysis, is not typically seen in patients with myocardial infarction.2 Second, in several cases, coronary angiography failed to reveal the slow-flow phenomenon, even in the presence of ST-segment elevation. Finally, impaired microcirculation during the acute phase is not direct evidence of causation, because microcirculatory impairment can result from a primary myocardial injury.

Another putative mechanism is neurogenic stunned myocardium. This condition is also observed during acute cerebrovascular accidents16,17 and during the catecholamine-induced cardiomyopathy in patients withpheochromocytoma.18–20 Enhanced sympathetic activity appears to play a very important role in the pathophysiology of takotsubo cardiomyopathy. Triggering factors, such as intense emotional stress, are frequently seen in patients with this syndrome. Excessive levels of catecholamines have been observed in patients with takotsubo cardiomyopathy.2 Catecholamines have been shown to induce myocardial damage,21,22 and excessive stimulation of cardiac adrenergicreceptors has led to transient LV hypocontraction in animal models.23 A 2005 case series12 showed a strong relationship between stress-inducedcardiomyopathy and increased plasma catecholamine levels, suggesting that exaggerated sympathetic activation may be important in the development of thecardiomyopathy.

The possibility that myocarditis leads to transient LV dysfunction has also been suggested, but results of biopsies and paired serum tests for viral serology have been negative in the patients studied.2

Another intriguing question surrounding takotsubo cardiomyopathy is that of why the apical wall is affected but the base is spared. Several explanations have been proposed.8 The apex is structurally vulnerable because it does not have a 3-layered myocardial configuration, it has a limited elasticity reserve, it can easily become ischemic as a consequence of its relatively limited coronary circulation, and it is more responsive to adrenergic stimulation.24 All of these factors might make the apex more sensitive to the catecholamine-induced surge frequentlyobserved in takotsubo cardiomyopathy.

Transient intraventricular pressure gradients have also been detected in some patients diagnosed with takotsubo cardiomyopathy.2,8,10 However, the absenceof significant LV hypertrophy in takotsubo cardiomyopathy, along with thedistinctive histologic features, rules out the possibility of an acutemidventricular obstruction, as seen in patients who have hypertrophic cardiomyopathy.

Although short-term outcomes are excellent, with complete resolution in all reported cases,2,8,9,11 there are no data in the literature regarding long-term outcome in patients who have experienced takotsubo cardiomyopathy.

Takotsubo cardiomyopathy has important implications, because its clinical presentation mimics that of an acute coronary syndrome. Increased awareness of takotsubo cardiomyopathy will likely result in its being diagnosed more frequently. Prospective studies are needed in order to determine more accurately the incidence of takotsubo cardiomyopathy and to ascertain the long-term outcomes. Studies are also needed to elucidate the specific pathophysiologic mechanisms responsible for this cardiomyopathy.


Address for reprints: Salim S. Virani, MD, Division of Cardiology, Texas Heart Institute at St. Luke’s Episcopal Hospital, 6720 Bertner, P-332, Houston, TX 77030. E-mail: ude.cmt.mcb@inariv


1. Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases [in Japanese]. J Cardiol 1991;21:203–14. [ PubMed]
2. Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, Sasaka K. The clinical features of takotsubo cardiomyopathy. QJM 2003;96:563–73. [ PubMed]
3. Kurisu S, Sato H, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448–55. [ PubMed]
4. Shimizu M, Takahashi H, Fukatsu Y, Tatsumi K, Shima T, Miwa Y, et al. Reversible left ventricular dysfunction manifesting as hyperkinesis of the basal and the apical areas with akinesis of the mid portion: a case report [in Japanese]. J Cardiol 2003;41:285–90. [ PubMed]
5. Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42. [ PubMed]
6. Iga K, Hori K, Kitaguchi K, Matsumura T, Gen H, Tomonaga G, Tamamura T. Transient segmental asynergy of the left ventricle of patients with various clinical manifestations possibly unrelated to the coronary artery disease. Jpn Circ J 1991;55:1061–7. [ PubMed]
7. Akashi YJ, Sakakibara M, Miyake F. Reversible left ventricular dysfunction “takotsubo” cardiomyopathy associated with pneumothorax. Heart 2002;87:E1. [ PMC free article] [ PubMed]
8. Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11–8. [ PubMed]
9. Seth PS, Aurigemma GP, Krasnow JM, Tighe DA, Untereker WJ, Meyer TE. A syndrome of transient left ventricular apical wall motion abnormality in the absence of coronary disease: a perspective from the United States. Cardiology 2003; 100:61–6. [ PubMed]
10. Bybee KA, Prasad A, Barsness GW, Lerman A, Jaffe AS, Murphy JG, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343–6. [ PubMed]
11. Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [ PubMed]
12. Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48. [ PubMed]
13. Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472–9. [ PubMed]
14. Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003; 89:1027–31. [ PMC free article] [ PubMed]
15. Ako J, Takenaka K, Uno K, Nakamura F, Shoji T, Iijima K, et al. Reversible left ventricular systolic dysfunction–reversibility of coronary microvascular abnormality. Jpn Heart J 2001;42:355–63. [ PubMed]
16. Pollick C, Cujec B, Parker S, Tator C. Left ventricular wall motion abnormalities in subarachnoid hemorrhage: an echocardiographic study. J Am Coll Cardiol 1988;12:600–5. [ PubMed]
17. Sakamoto H, Nishimura H, Imataka K, Ieki K, Horie T, Fujii J. Abnormal Q wave, ST-segment elevation, T-wave inversion, and widespread focal catalysis associated with subarachnoid hemorrhage. Jpn Circ J 1996;60:254–7. [ PubMed]
18. Yamanaka O, Yasumasa F, Nakamura T, Ohno A, end Y, Yoshimi K, et al. “Myocardial stunning” -like phenomenon during a crisis of pheochromocytoma. Jpn Circ J 1994;58: 737–42. [ PubMed]
19. Salathe M, Weiss P, Ritz R. Rapid reversal of heart failure in a patient with phaeochromocytoma and catecholamine-induced cardiomyopathy who was treated with captopril. Br Heart J 1992;68:527–8. [ PMC free article] [ PubMed]
20. Scott IU, Gutterman DD. Pheochromocytoma with reversible focal cardiac dysfunction. Am Heart J 1995;130:909–11. [ PubMed]
21. Mann DL, Kent RL, Parsons B, Cooper G 4th. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation 1992;85:790–804. [ PubMed]
22. White M, Wiechmann RJ, Roden RL, Hagan MB, Wollmering MM, Port JD, et al. Cardiac beta-adrenergic neuroeffector systems in acute myocardial dysfunction related to brain injury. Evidence for catecholamine-mediated myocardial damage. Circulation 1995;92:2183–9. [ PubMed]
23. Ueyama T, Kasamatsu K, Hano T, Yamamoto K, Tsuruo Y, Nishio I. Emotional stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors: a possible animal model of ‘tako-tsubo’ cardiomyopathy. Circ J 2002;66:712–3. [ PubMed]
24. Mori H, Ishikawa S, Kojima S, Hayashi J, Watanabe Y, Hoffman JI, Okino H. Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli. Cardiovasc Res 1993;27:192–8. [ PubMed]
Articles from Texas Heart Institute Journal are provided here courtesy of Texas Heart Institute

ga('send', 'pageview');
The Braindoc's Blog
%d bloggers like this: