Cardiovascular Manifestations in Patients With Thrombotic Thrombocytopenic Purpura: A Single‐center Experience

Abstract

Background: Cardiovascular manifestation in patients with thrombotic thrombocytopenic purpura. Hypothesis: The aim of this study was to investigate the incidence of acute myocardial infarction (AMI), arrhythmias, congestive heart failure, and mortality in patients hospitalized for thrombotic thrombocytopenic purpura (TTP). Methods: Thirty-eight patients (27 women and 11 men), mean age 44 years, were hospitalized with the diagnosis of TTP confirmed by a hematologist. We investigated the incidence of AMI which developed during hospitalization for TTP. AMI was diagnosed by new electrocardiographic changes, increased serum cardiac troponin I levels, and clinical symptomatology. The patients with AMI were also monitored for development of arrhythmias during hospitalization. Results: Of the 38 patients, 8 (21%) developed new Q-wave AMI. There was no significant difference in baseline characteristics between patients who developed AMI and those who did not develop AMI. Of the 8 patients with AMI, 2 (25%) developed atrial fibrillation, 1 (13%) developed atrial flutter, 1 (13%) developed supraventriculartachycardia, and 2 (25%) developed congestive heart failure. Death occurred in 3 of 8 patients (38%) with AMI and in 1 of 30 patients (3%) without AMI (P < 0.01). Conclusions: New Q-wave AMI developed in 21% of 38 patients hospitalized with TTP. Supraventricular tachyarrhythmias developed in 50% of 8 patients with TTP who developed AMI. Patients hospitalized for TTP should be monitored for adverse cardiac events due to the high incidence of new AMI, supraventricular tachyarrhythmias, and mortality.

Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

“…One of the typical signs of TTP is MI/R injury, suggesting a link between low ADAMTS13 activity and MI/R injury. [12][13][14][15][16] Clinical studies revealed that low ADAMTS13 (and high VWF) levels are associated with an increased risk of MI. 6,[17][18][19][20][21][22] ADAMTS13 polymorphisms that decrease ADAMTS13 activity are also associated with an increased risk of death in patients with coronary artery Figure 2.…”

Thrombotic Thrombocytopenia Purpura: A Potentially Reversible Cause of Complete Heart Block

“…4 Even within the heart, the presentation of thrombotic complications are diverse. [5][6][7] A systemic review showed that, of 111 patients with cardiac involvement, 26 had myocardial infarctions, 17 had congestive heart failure, 10 had arrhythmias, 6 had cardiogenic shock, and 8 had sudden cardiac death. 8 Cardiac arrhythmias are reported less frequently in thrombotic thrombocytopenia purpura, yet there are reports of a wide range of anomalies.…”

“…8 Another study reported that 4 of 8 patients with thrombotic thrombocytopenia purpura and myocardial infarctions developed atrial fibrillation, atrial flutter, and supraventricular tachycardias. 6 While rarely reported in patients who survive this deadly disorder, cardiac conduction abnormalities have been recognized widely in postmortem studies. Ridolfi et al 9 reported on 17 patients with thrombotic thrombocytopenia purpura who died due to disease complications.…”

Cardiac involvement in thrombotic microangiopathies

“…Однако, как и при ТТП, описаны выпот в полость перикарда с тампонадой сердца, нарушения ритма и проводимости, кардиогенный шок, синкопальные состояния, не связанные с поражением легких и ЦНС, а также внезапная смерть [3,32,36]. Последняя, по-видимому, также может быть обусловлена аритмиями, поскольку при аутопсийном исследовании миокарда умерших пациентов с ТТП выявлен тромбоз сосудов в области атриовентрикулярного узла и пучка Гиса [7,37,38]. Морфологическая картина пораже-ния миокарда при обоих заболеваниях также не различается на светооптическом уровне: гистопатологическое исследование вы-являет очаги некроза миокарда, утолщение стенки мелких сосу-дов, отек ЭК, расширение субэндотелия, интралюминальные тромбы.…”